Gastroesophegeal Reflux and Gastritis Oct 02, 2024

In this episode of PEM Currents: The Pediatric Emergency Medicine Podcast, I explore the complexities of gastroesophageal reflux (GER) and gastritis in children and adolescents. I’ll make the important distinction between gastritis – which is diagnosed only via endoscopy – and dyspepsia, the term best used to describe the symptoms many patients experience. I’ll dive into the latest clinical practice guidelines and discuss evidence-based approaches to diagnosis and treatment.

Topics covered include:

The pathophysiology of GER and GERD in the pediatric population.
Understanding dyspepsia and its clinical presentation.
Diagnostic strategies and when to consider further evaluation.
The role of lifestyle and dietary modifications in management.
Pharmacological interventions, including the use of proton pump inhibitors (PPIs), H2 blockers, and antacids.
Current controversies and updates in pharmacological treatments.
Management of gastritis and the consideration of Helicobacter pylori infection.

Join me as I scope out the nuances of gastroesophageal reflux and gastritis and provide practical insights for clinicians in the emergency setting.

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References

Rosen R, Vandenplas Y, Singendonk M, et al. Pediatric Gastroesophageal Reflux Clinical Practice Guidelines: Joint Recommendations of the North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition and the European Society for Pediatric Gastroenterology, Hepatology, and Nutrition. J Pediatr Gastroenterol Nutr. 2018;66(3):516-554. doi: 10.1097/MPG.0000000000001889

Lightdale JR, Gremse DA; Section on Gastroenterology, Hepatology, and Nutrition. Gastroesophageal Reflux: Management Guidance for the Pediatrician. Pediatrics. 2013;131(5):e1684-1695. doi: 10.1542/peds.2013-0421

Tighe M, Afzal NA, Bevan A, et al. Pharmacological Treatment of Children with Gastro-oesophageal Reflux. Cochrane Database Syst Rev. 2014;2014(11):CD008550. doi: 10.1002/14651858.CD008550.pub2

Sintusek P, Mutalib M, Thapar N. Gastroesophageal Reflux Disease in Children: What’s New Right Now? World J Gastrointest Endosc. 2023;15(3):84-102. doi: 10.4253/wjge.v15.i3.84

Transcript

Note: This transcript was partially completed with the use of the Descript AI

Welcome to PEMCurrents, the pediatric emergency medicine podcast. As always, I’m your host, Brad Sobolewski, and today’s episode will focus on gastro esophageal reflux and gastritis in children and adolescents. Both conditions can present with similar symptoms. They do, though, have distinct pathophysiologies and management strategies.

So we’re going to discuss the evidence based approaches to diagnosis and treatment, and I will talk about why it is presumptive to call things gastritis before definitive diagnosis, even though I put it in the title of the episode. Alright, let’s scope things out. I’m going to begin by making a brief distinction between gastroesophageal reflux and gastroesophageal reflux disease.

So, reflux itself is a common physiologic process, especially in infants, that usually resolves by 12 to 18 months, when the gastroesophageal sphincter gets tighter, and kids spend more of their life on it. upright. Gastroesophageal reflux disease is when the patients have severe symptoms that persist and cause long term issues.

Now, either way, this is due to reflux of the stomach contents into the esophagus. Now, gastroesophageal reflux is incredibly common in infants with up to 50 percent of b cells. babies under three months regurgitating daily. This typically peaks at about four months of age and improves as the infant grows.

Gastroesophageal reflux disease is less common, but still affects about 10 percent of children and up to 10 to 20 percent of adolescents. Adolescents with GERD often present similarly to adults with heartburn and regurgitation as the primary complaints. Now there are some risk factors for GERD.

Gastroesophageal reflux and reflux disease in children. A main one is neurological impairment. So kids with cerebral palsy or other neurologic disorders have delayed gastric emptying and poor esophageal motility, increasing the risk of GERD. Children with respiratory conditions and chronic lung disease like asthma are more prone to GERD as well.

And reflux itself can exacerbate the existing respiratory symptoms either through microaspiration or vagal mediated bronchospasm. Prematurity and congenital conditions like esophageal atresia also obviously increase the risk. So gastroesophageal reflux and reflux disease result from transient relaxation of the lower esophageal sphincter.

That allows acidic gastric contents to flow back into the esophagus. Now, the lower esophageal sphincter is supposed to prevent this reflux from happening. In GERD, the sphincter relaxes too frequently or incompletely, which can lead to symptoms building up over time. Other factors like delayed gastric emptying and abnormal esophageal motility can worsen problems in general.

And the presentation for GERD varies by age. Infants will have frequent spitting up or vomiting after feeds, irritability during or after feeds, especially in the more significant cases where the esophagus is irritated. Uh, infants may start to refuse to feed due to the discomfort. They can have poor weight gain or even failure to thrive in more severe cases.

And they can have Sandefur syndrome, which is the arching of the back and dystonic posturing that occurs during or after feeds as a response to discomfort from acid reflux. This is sometimes misidentified as seizures. In older children and adolescents, heartburn is the most common symptom. It’s a burning sensation in the chest or epigastrium, and that is the classic symptom in this age group.

You can also see regurgitation, acid or food regurgitating into the mouth, leading to a sour taste. uh, ill defined epigastric or chest pain, and it’s often worse by eating or lying down after meals. And some other symptoms that you gotta think about in reflux, chronic cough, hoarseness, or even asthma like symptoms.

These extra esophageal manifestations can occur due to irritation of the upper airways by the gastric contents. Now, in the pediatric emergency department, the diagnosis of reflux is primarily clinical. You just got to take a good history and do a physical examination, especially when the symptoms are typical, like regurgitation, heartburn, or epigastric pain in an older child or adolescent.

You want to take a good history on feeding or dietary habits. In infants, you want to know the amount and frequency of feeding, especially because baby stomachs are small and no newborn stomach can hold six ounces. So, the parents may say, well, he Doesn’t ever seem full. Well, baby doesn’t know how to be full.

So really, you need to learn how much a baby can take and follow weight gain appropriately. Overfeeding a baby will lead to increased spitting up and reflux. You should also ask about older children and adolescents eating trigger foods like spicy things, caffeinated beverages, and acidic beverages like pop.

These can all exacerbate reflux. You want to ask about nocturnal symptoms. So if the kid has symptoms that are worse at night or immediately upon waking up, this may indicate reflux exacerbated by lying down, especially after meals. Red flags that you should always ask about include hematemesis, melana, dysphagia, and Unintentional weight loss, these all need further investigation for complications like esophagitis or another diagnosis such as EOE or peptic ulcer disease.

If any of those red flags are present, you should definitely consider a further diagnostic workup. Again, otherwise the diagnosis is based on history and physical examination. So if you see failure to thrive or poor weight gain, again, vomiting blood or passing black tori stools, signs of esophagitis such as painful swallowing or difficulty swallowing.

They need more workup often via GI. So diagnostic testing centers around endoscopy. That’s the gold standard and ultimately getting a camera in there. Taking a look for strictures or ulcers and taking a biopsy of the esophageal and gastric mucosa will make the diagnosis and evaluate for other things like eosinophilic esophagitis or helicobacter pylori infection.

Also get a pH monitoring and impedance probe. This measures both acid and non acid reflux events. It’s kind of like a Holter monitor for reflux. This is obviously ordered by a gastroenterologist, but But the probe itself measures reflux, and then the patient can press a button for an event monitor. And this is particularly useful in children with atypical symptoms or extra esophageal manifestations like cough or asthma, and especially in those that have had a normal endoscopy.

Contrast radiography, like a barium swallow, has much lower sensitivity and specificity than scopes or, in certain situations, even impedance probes and pH monitors. Now, that being said, imaging can be helpful if you suspect hypertrophic pyloric stenosis or other causes of obstruction such as duodenal atresia or antral webs.

But again, you should suspect these based on a detailed history and physical. A management of gastroesophageal reflux is largely dependent on the severity of symptoms and the patient’s age. And most cases of GERD in a pediatric ED can be managed conservatively with feeding or lifestyle modifications and short term pharmacotherapy.

So in infants, you want to recommend smaller, more frequent feeds. Again, overfeeding is a common contributor to reflux in infants. Maybe parents will have to thicken the feeds, but I do not recommend this in the emergency department. Um, and this practice adds rice cereal to the formula or express breast milk that may reduce regurgitation.

Again, this should only really be done under supervision of the child’s pediatrician, keeping infants upright for a half hour after feeds, can let gravity be your friend and reduce reflux episodes. And in older Children and adolescents, the first and most important thing to do is to do dietary modifications like avoiding trigger foods, caffeine, chocolate, spicy foods and acidic beverages like pop.

Large fatty meals should also be avoided, especially in the two to three hours before bedtime. You should encourage older children to avoid lying down immediately after meals, and in some cases, elevating the head of the bed by 30 degrees can reduce night time symptoms. If you feel that you do need to do pharmacologic management, The most effective drugs are proton pump inhibitors like omeprazole and lansoprazole.

They can reduce gastric acid production and help heal the esophagus. A 4 8 week trial of PPIs is recommended for children with moderate to severe GERD, especially those with esophagitis. So you could start that in the emergency department if the symptoms are severe enough, provided that they have primary doctor follow ups.

You may need to wean these PPIs off if symptoms improve because long term use could be associated with risks such as malabsorption of calcium and magnesium or maybe even an increased risk of GI infections such as C. difficile. H2 blockers or H2 formatidine can be used as an alternative to PPIs in milder cases of GERD.

They start working faster. Again, the PPI’s take three to four days to start working. H2’s work immediately. They do reduce acid production to a lesser degree. In older children and adolescents, antacids can provide symptomatic relief of heartburn, but they don’t address underlying acid production. And then there’s things for infants like myelocon and gas drops.

And if you want to try them, go ahead, but they ain’t gonna stop the physiologic process of reflux. And I’ll touch on surgical management briefly before moving on to part two. In rare, severe cases where GERD is refractory to medical management, surgical interventions like fundoplication may be considered, especially in kids with neurologic impairments or life threatening aspiration.

All right, let us shift gears to gastritis. So gastritis is inflammation of the gastric mucosa and can result from infections such as H. pylori, H. pylori, medication overuse, particularly NSAIDs or other stressors. Children with gastritis often present with epigastric pain, nausea, and vomiting, particularly after meals.

And yes, these symptoms do overlap with gastroesophageal reflux and gastroesophageal reflux disease, but they are separate entities. Now there’s a big caveat here. I know that I’m using the word gastritis. And it’s even in the title of the episode. But technically, this diagnosis is only made after endoscopy and biopsy.

Trust me, I asked a gastroenterologist about this directly. So therefore, if you’re seeing this kid for the first time and there’s no established diagnosis, it’s more accurate, especially when an endoscopy has not yet happened, to diagnose them and label that diagnosis based on their symptoms, such as abdominal pain, nausea, early satiety, endoscopy.

Or, you can label it as dyspepsia, also known as indigestion. This refers to a condition characterized by discomfort or pain in the upper abdomen. Typically manifests as fullness, bloating, nausea, or burning in the stomach, especially after eating. And as noted throughout this episode, dyspepsia can be caused by several factors that overlap with GERD and even a kid who gets an ultimate diagnosis of gastritis, like overeating, spicy or fatty food, stress, or underlying conditions.

And technically, the most common cause is functional dyspepsia. Now, I know that’s a lot to digest, and you might be starting to churn, but let’s talk now about the relationship between eating and pain. A key feature of gastritis is the timing of pain. Pain in gastritis typically occurs shortly after eating, as food stimulates gastric acid production, which can irritate the inflamed stomach lining.

You want to ask detailed questions about the timing in pain in relation to meals. Again, that pain is mostly shortly after eating. The foods that cause more symptoms are the ones you’d expect. Spicy, fatty, acidic, or caffeinated items. A detailed dietary history is one of the first steps to making the diagnosis.

You also want to take a detailed history of medication use, especially NSAIDs. Chronic NSAID use for often comorbid symptoms such as headache can damage the gastric mucosa leading to gastritis. The red flag symptoms, as expected, are similar to GERD. Look for signs of GI bleeding, such as hematemesis or melanoma.

or somebody who appears pale, dehydrated, in severe pain, or worse, even in shock. So if you think a kid has dyspepsia, or maybe even eventually gastritis, it’s the history and physical alone which will make the diagnosis. Now a GI cocktail, which is antacid plus viscous lidocaine, could modify the patient’s current symptoms and help sort of convince them where the pain is coming from.

It has been called into question recently by the adult literature. And probably with good cause, as In an older adult with GI symptoms, you should be worried about myocardial infarction or other causes and if you alleviate or mask the pain then you may be moving yourself away from a more important diagnosis.

There also is the worry about rapid systemic absorption of the lidocaine. In general, I’ve not found them to be incredibly helpful in children, but if you’re not worried about other causes, and you need to modify the kid’s pain to sort of help them convince that it’s their stomach and esophagus as a source of the pain, then it could be worth trying.

I mentioned again that the diagnosis is based on history and physical. If they’ve been dealing with chronic symptoms, And there’s an abrupt worsening, or again, the child has red flag symptoms, then you probably do want to get some labs, such as the CBC, check the HNH, lipase, renal panel, liver profile, and ESR and CRP.

Like a kid with normocytic anemia and an ESR of 140, that ain’t gastritis. I’d be worried about inflammatory bowel disease, for instance. Plain films are generally not helpful unless you suspect obstruction or foreign body ingestion. And then, only a radiopaque foreign body. A CT scan can show some signs of liver disease or pancreatitis, but the HNP followed by targeted labs is a more safe and judicious approach.

Now, ultrasound is useful if you suspect gallbladder disease, but the patient needs to be NPO for six to eight hours before the procedure. This will that the gallbladder is distended, which improves the accuracy of the ultrasound in visualizing gallstones or sludge or other abnormalities. So, a kid with mild symptoms, and you want to rule out gallbladder disease?

Like, you can totally order this as an outpatient. You don’t need to make them wait in the ED for six to eight hours. Have a detailed discussion with the patient and family and do shared decision making in terms of interventions, the GI does, and again, these will be the gold standards. Endoscopy, upper GI and endoscopy is the gold standard for diagnosing gastritis.

You see direct visualization of the gastric mucosa and you take biopsies, which can rule out helicobacter pylori or eosinophilic esophagitis or eosinophilic gastritis. Non invasive H. pylori testing, like stool antigens or a urea breath test, can be helpful for diagnosing H. pylori, especially in cases of chronic or recurrent symptoms.

But, being on a PPI can make these tests less accurate. So really, scope is still the way to go. In the end, the most common diagnoses are All of these kids with gastritis like symptoms are going to end up is functional dyspepsia. This is chronic or recurrent pain and discomfort centered in the left upper abdomen without any identifiable structural or biochemical abnormalities upon medical examination.

Gastritis is, once again, inflammation of the stomach lining, which is only truly identified with endoscopy and biopsy. And yes, I called this episode gastroesophageal reflux and gastritis because it’s a colloquial term, but it’s important to make the distinction that ultimately these kids should be labeled as their symptom or dyspepsia in the ED and then followed up with their primary doctor or GI if necessary.

And many of us will ask about H. pylori. And it’s more common in adults, but it’s actually pretty rare in kids. So unless someone living in the home with a kid has an active infection is being treated. it’s probably not going to be H. pylori in the kid. And still, GI would recommend that we don’t start empiric antibiotic treatment in the emergency department anyway, because it’s best to diagnose that with a scope.

So in the odd, rare scenario where you have a family member being treated for H. pylori and a kid with symptoms, I wouldn’t actually start them on a PPI and instead refer to GI for definitive diagnosis. Other things on the differential include peptic ulcer disease, Again, that’s something that really you’ll pick up on endoscopy, but a kid looks like they’re bleeding out, I’d be worried about it, and they are coming in.

It’s also worth mentioning that gastroparesis and delayed gastric emptying can also cause symptoms of dyspepsia. So what are some other important causes of abdominal pain that you should differentiate from dyspepsia and gastritis? And by differentiate, I mean both ask the right questions and tell the family that you are not worried about them.

First, pancreatitis. So the pain in pancreatitis is typically more severe, constant, can radiate to the back, unlike the more intermittent pain of gastritis. Patients will have more nausea and vomiting and some systemic signs like fever or tachycardia. Elevated lipase can make the diagnosis, though Ultrasound or CT can show some pancreatic inflammation.

Gallstones can be seen in adolescence. Pain in the right upper quadrant or epigastric pain. It’s often described as colicky, worsened by fatty meals. Ultrasound, as I noted before, is the diagnostic test of choice. And peptic ulcer disease from duodenal ulcers improves with food, but then worsens several hours later.

Whereas gastric ulcers may worsen shortly after eating, similar to gastritis. Endoscopy will make the diagnosis. And then there’s celiac disease. So celiac disease can cause dyspepsia symptoms as well. Celiac disease is a true autoimmune disorder triggered by the ingestion of gluten. It’s a protein found in wheat, barley, and rye.

In individuals with celiac disease, gluten intake leads to an immune mediated inflammatory response that damages the small intestine’s mucosal lining, specifically the villi. It kind of blunts them down. This impairs nutrient absorption and can lead to a variety of GI symptoms. So if somebody says, I’m not eating gluten because I don’t feel like it or because I want better hair.

Maybe I should try that. That’s not celiac disease. Celiac disease is an immune process. So dyspepsia is a symptom that can occur in celiac disease, and so if you take a history that things worsen upon eating gluten, or what happens if the patient has eliminated gluten from their diet, which is something that I’ve seen many families do on their own.

And it’s not within the scope of this episode, but the anti tissue transglutaminase antibodies, TTG, IgA, that’s the most sensitive and specific initial test for celiac. All right, let’s start to talk about now the management of dyspepsia and gastritis. Dietary and lifestyle changes are the first line treatment.

They can significantly improve symptoms. It’s important that we communicate to patients and families how optimistic we are that these can make a difference. So avoid trigger foods, spicy and fatty foods, acidic foods and beverages like citrus fruits and carbonated drinks. Caffeine and chocolate, and even dairy products if you suspect lactose intolerance.

You want to encourage eating of small, frequent meals. That allows you to digest the gastric contents a little more efficiently. Chew your food thoroughly. Don’t swallow things like a snake. That reduces the swallowing of air and aids digestion. And avoid late night eating, especially two to three hours before bedtime.

No bedtime snacks for these kids. Kids should stay well hydrated, adequate water intake, and limit sugary drinks like juice and pop that can irritate the stomach. Gatorade. That’s a big offender that I’ve run up against. Stress management is really important because stress can exacerbate symptoms, deep breathing, meditation, biofeedback, regular physical activity promotes healthy digestion, and avoiding secondhand smoke because tobacco smoke can irritate the stomach lining.

If you want some symptomatic relief, you can use antacids. They neutralize stomach acid and provide quick relief from symptoms. So Tums, or calcium carbonate, you chew it and it neutralizes existing stomach acid. It’s quick, short term relief. If you take way too many of them, you can get constipation or hypercalcemia.

Maalox, which is aluminum hydroxide and magnesium hydroxide, it’s two antacids, and it can balance side effects maybe, I don’t know. That also provides symptomatic relief. It’s a little bit gritty, but you drink it. And there are pediatric formulations. If you take a lot of it, magnesium can cause diarrhea, and aluminum can cause constipation.

I don’t know if those balance out at all. I haven’t tried it. Then you have your H2 receptor antagonists, or H2 blockers. These medications reduce stomach acid production by blocking histamine receptors in the stomach lining cells. So you’ve got things like famotidine or pepsid. Runitidine or Zantac was commonly used, but it’s been withdrawn from the market due to some safety concerns.

Lomatidine will decrease acid secretion, and it’s effective for mild to moderate symptoms, and it starts shortly after taking it, and is generally well tolerated. The next step up are proton pump inhibitors. These are more potent acid suppressants, and they block the enzyme responsible for acid secretion itself, as opposed to just the pump.

You’ve got drugs like Prilosec, which is Omeprazole, Prevacid, which is Lansoprazole, or Nexium, Esomeprazole. They all work fine and there’s some pediatric formulations which you can look up and sometimes insurances will take one and not the other, again, beyond the scope of this episode. These are prescribed for more severe symptoms or when H2 blockers are ineffective.

Follow pediatric weight based dosing and know that it does take three to four days before the suppression starts working. Long term use could affect nutrient absorption of like magnesium or vitamin B12. And being on a PPI as opposed to being on an H2 blocker can, as I mentioned earlier, alter the results of an endoscopy.

So if you think a kid’s going to need a scope, don’t start a PPI. Or you can stop the PPI if they’re going to get a scope within the next one to two weeks. Let me talk about one more medication that I’ve used occasionally. And so it’s sucrophate or carophate. This kind of acts like a protective barrier over the stomach lining that can aid in healing.

It’s kind of like putting, like, spackle over the stomach. It just kind of blocks everything up and tamps down the symptoms. It’s a viscous, adhesive substance, and it can adhere to ulcer sites as well. This is really short term treatment for more severe pain. You would administer this on an empty stomach, usually an hour before meals, or when a child is having severe symptoms not around the time of meals.

If you use a lot of it, it can cause constipation or interfere with the absorption of other daily medications. So fortunately, most of the kids with dyspepsia, or kids that you think will ultimately be diagnosed with gastritis, will be able to be discharged home. So first and foremost, recommend dietary and lifestyle modifications.

For You could start a daily proton pump inhibitor and explain to the family that it takes three to four days before it starts working. If they want more immediate relief or the symptoms are mild, you consider using an H2 blocker instead. For mild intermittent symptoms, consider adding Tums if they like to chew a tablet or Maalox if they’d rather drink a liquid.

And for a step up to more severe symptoms, suggest the use of sucrophate and intermittently and judiciously. You should have the child follow up with their primary care doctor often after about 10 to 14 days on the acid blocking regimen that you prescribed. If they’re doing better and they’ve made diet and lifestyle modifications, the primary doctor at that point can discuss how long to maintain therapy and develop an exit strategy.

A trial of four to eight weeks would be reasonable. But if they’re not improving, And that could be a cause for referral to gastroenterology. It’s important in the ED to not over promise that, oh yeah, you’re going to see GI. Kids can get better on what we recommend. You should trust that. So don’t immediately refer to GI unless you’re worried about a bleeding ulcer or another diagnosis like inflammatory bowel disease or celiac or eosinophilic esophagitis because every time they swallow chicken and steak it gets stuck in their esophagus.

Remember, our community pediatricians, family medicine doctors, are brilliant. They can handle this problem. But if a child has those red flags, or if you’re concerned they need immediate intervention, by all means, get them to a pediatric center for admission and GI evaluation imminently. And again, I will say it yet one more time, because most of these kids have not yet had endoscopy with biopsy, I would not recommend using the diagnosis gastritis.

And I did put it in the title, but it’s what most people call it, and perhaps this was a bridge to education. Use symptoms as your diagnosis. Abdominal pain, nausea, early satiety, or probably most appropriately, call it dyspepsia. These kids are having indigestion. Don’t minimize it. It is having a significant impact on their daily lives.

They kept whining about it. They came to the ED. And it is tempting to call it gastritis because it seems more significant or impactful, but Avoiding making a presumptive diagnosis does not minimize the symptoms the child is having. Instead, use this as a teachable moment and link your interventions with your expected symptom improvement.

Alright, so we know that gastroesophageal reflux and gastritis are linked. really dyspepsia, are common yet distinct causes of GI symptoms in pediatric patients. Recognizing the key features of these conditions and differentiating them from other causes of epigastric pain, such as pancreatitis, gallstones, and ulcers, is crucial in providing appropriate management.

Thank you for listening to this episode. I hope you were able to pick up some new pearls that you can take back to your next clinical shift. If you have any feedback on this episode or would like to suggest content for a future episode, send it my way. I’ll take an email, a comment on the blog, a direct message on X or another social media platform.

And my kids will remind me to say, like, rate, and review. That’s so more people can find the show and continue to learn. For PEM Currents, the Pediatric Emergency Medicine Podcast, this has been Brad Sobolewski. See you next time.

ECPR Aug 20, 2024

This episode of PEM Currents discusses ECPR (Extracorporeal Cardiopulmonary Resuscitation), an advanced procedure used in cases of cardiac arrest when traditional CPR fails. ECPR involves using ECMO (Extracorporeal Membrane Oxygenation) to take over heart and lung functions, offering a last-resort option that is becoming more common in large pediatric hospitals. While ECPR shows promise in improving survival rates, particularly in pediatric patients with conditions like congenital heart disease, it is resource-intensive and carries significant risks. Establishing an ECPR program requires robust infrastructure, multidisciplinary teamwork, and extensive training. The episode highlights the importance of understanding eCPR as a critical therapy for both in-hospital and out-of-hospital cardiac arrests.

PEMBlog

@PEMTweets on… sigh “X” (Twitter)

My Instagram

My Mastodon account @bradsobo

References

Gajkowski EF, Herrera G, Hatton L, et al. ELSO guidelines for adult and pediatric extracorporeal membrane oxygenation circuits. ASAIO J. 2022; 68:133–152.

Stratton, M., & Edmunds, K. (2024). Extracorporeal Cardiopulmonary Resuscitation. Pediatric Emergency Care, 40(8), 618-622.

ECC Committee, Subcommittees, and Task Forces of the American Heart Association. 2005 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2005;112(suppl):IV1–IV203.

Yannopoulos D, Kalra R, Kosmopoulos M, et al. Rationale and methods of the advanced R2Eperfusion STrategies for refractory cardiac ARREST (ARREST) trial. Am Heart J. 2020;229:29–39.

Bartos JA, Yannopoulos D. Starting an extracorporeal cardiopulmonary resuscitation program: success is in the details. Resuscitation. 2023; 187:109792.

Syphilis Jul 10, 2024

Syphilis has gone by many nicknames over the years including “The Great Pretender” and “The Great Imitator.” Emily Labudde, MD, a Pediatric Emergency Medicine fellow at Children’s Healthcare of Atlanta and recent pediatric residency graduate from Cincinnati Children’s discusses the various manifestations of this sexually transmitted infection, and how we can’t miss this very treatable, but sneaky malady.

PEMBlog

@PEMTweets on… sigh “X” (Twitter)

My Instagram

My Mastodon account @bradsobo

References

Emily J. Labudde, Jane Lee; A Review of Syphilis Infection in Pediatric Patients. Pediatr Rev. July 2024; 45 (7): 373–380. https://doi.org/10.1542/pir.2023-006309

Centers for Disease Control and Prevention. “Sexually Transmitted Disease Surveillance 2021.” Centers for Disease Control and Prevention, 2021. Available from: https://www.cdc.gov/std/statistics/2021/default.htm.

Centers for Disease Control and Prevention. “Sexually Transmitted Infections Treatment Guidelines 2021.” Centers for Disease Control and Prevention, 2021. Available from: https://www.cdc.gov/std/treatment-guidelines/syphilis.htm.

Centers for Disease Control and Prevention. “Youth Risk Behavior Surveillance System.” Centers for Disease Control and Prevention, 2021. Available from: https://www.cdc.gov/healthyyouth/data/yrbs/index.htm.

Transcript

Note: This transcript was partially completed with the use of the Descript AI

Welcome to PEMCurrents, the Pediatric Emergency Medicine Podcast, as always, I’m your host Brad Sobolewski. Today’s episode is all about the great pretender, syphilis. And let’s face it, it’s not just a disease for Medieval royalty. It’s on the rise in the United States and abroad. So let’s talk about the manifestations and management.

And I’ve got a special guest host. This is Emily Labudde, originally from Detroit, at the time of recording this episode, a third year categorical pediatric resident at Cincinnati Children’s and a soon to be pediatric emergency medicine fellow in Atlanta. I’m going to pass the mic to you, Emily. My name is Emily Labudde, and I’m a third year pediatric resident at Cincinnati Children’s Hospital, and I’ll be starting fellowship in pediatric emergency medicine this summer at Emory University Children’s Healthcare of Atlanta.

Today’s podcast is going to cover acquired syphilis infection. Now, I know what you’re thinking. We don’t see a lot of syphilis in the pediatric ED. That’s what I thought, too, until I saw it, and with syphilis on the rise, it’s likely we’ll start to see more. I recently published a review article on syphilis in Pediatrics in Review, which you should check out.

It is far more detailed and also covers congenital syphilis, which is beyond the scope of this episode. At the end of this podcast, you should be able to appreciate the rising incidence of syphilis in the United States, especially amongst young people, recognize various signs and symptoms associated with different stages of syphilis infection, and identify the appropriate workup for possible syphilis infection, including co infections.

Syphilis is fondly referred to as the great imitator because of its various presentations. Headache? Could be syphilis. Rash? Could be syphilis. Weight loss? Could be syphilis. Epitrochlear lymphadenopathy? That’ll be on your boards. Definitely syphilis. I bet I could argue to have syphilis on every differential in some way, shape, or form.

But there are certain clues that can help guide you toward a more reasonable consideration of syphilis infection. Thank you, Jen. The U. S. is seeing a lot more cases of syphilis over the last decade or so. And, since we know from the CDC’s Youth Risk Behavior Survey that many American teens are having sex with less than optimal condom use and infrequent STI testing, pediatricians everywhere should be thinking more about acquired syphilis infection, not just congenital syphilis.

There are three stages of syphilis infection. Primary syphilis is often missed as it presents as a painless genital ulcer. Secondary syphilis causes systemic symptoms such as fever, anorexia, headache, malaise, lymphadenopathy, arthralgias, and rash, that classic rash on the palms and soles. It’s worth looking at a variety of pictures of this rash, some examples of which we have included in the show notes, as its appearance can vary, especially between different skin colors.

Tertiary syphilis is rare, and you’re almost guaranteed not to see it in a pediatric ED as it develops decades after initial infection. It’s characterized by gummas, which are granulomatous soft tissue tumors seen most often in the liver, but also in the bone, brain, heart, skin, testis, and eyes, and end organ damage, particularly of the central nervous system.

At any stage, patients can develop neurosyphilis, that can present with vision changes, neuropathies, seizures, or altered mental status. You may have heard this once or twice before, but your history and physical exam are so important, especially when looking for an infection like syphilis that can present in many different ways.

A thorough review of systems can help guide your differential and can point towards co infections with other STIs. Brush up on your sexual history taking skills because they’re critical here. This includes all the details like who has what parts and where they put them. Teens are awkward and they get super nervous when you kick out mom and dad and ask them what they’ve been doing on the weekends, but you won’t fully understand your patient’s risks without asking these questions.

It’s good preparation prior to the physical exam, which, you guessed it, should be thorough. We’re talking full body skin exam, neuro exam, genital exam, and all of the lymph nodes. Now, it would be really nice if our patients came in saying, Hey, my partner has syphilis, please test me for syphilis. And, like we talked about, syphilis can look like a lot of different things, so it’s important to keep your differential broad.

Syphilis testing can be divided into two types, treponemal and non treponemal. You’ll want to start with a non treponemal test, such as an RPR or VDRL. The RPR or Rapid Plasma Reagent, which has now largely replaced the earlier VDRL or Venereal Disease Research. Laboratory Test is a non-specific serological test for syphilis that uses CARDIOLIPIN as antigen.

These are highly sensitive tests. But watch out for false positives. The RPR is also useful for post treatment monitoring. Trepanemal tests, such as the FTA ABS, are used as confirmation in the setting of a positive non trepanemal test. Patients with neurologic complaints should undergo CSF testing as well.

And, of course, where there’s one, there’s probably more. Use the information from your very thorough sexual history to test your patient for any other STIs they are at risk for. Patients with primary or secondary syphilis can be treated with a single dose of benzathine penicillin G or a 14 day course of doxycycline if your patient has a penicillin allergy.

For any patient with tertiary or neurosyphilis or a pregnant patient with any stage of infection, 10 to 14 days of penicillin G is the only option, even in penicillin allergic patients. So, if a patient has a severe penicillin allergy, have rescue medications available. Watch out for that Gerrish Herxheimer reaction, I know you haven’t heard those words since medical school, which can cause fever, headache, myalgias, or nausea and vomiting in the first 24 hours after treatment.

Last, but not least, remember that in some cases you’re telling your patient about their disease and possibly some dishonesty from their partner. Be sure to counsel them on sharing their results with all of their sexual partners, as well as your responsibility to inform the local health department for disease tracking purposes and the option for third party partner notification.

A few brief points on congenital syphilis, which is covered more in depth in the review article. We most often see this in infants born to mothers with poor prenatal care, as our OB colleagues do a great job screening for syphilis multiple times during pregnancy. Most infants with congenital syphilis are asymptomatic at birth, with appearance of hepatomegaly, jaundice, copious rhinorrhea, lymphadenopathy, and a similar maculopapular rash on their hands and feet that develop later in infancy.

Think about congenital syphilis in your little ones presenting like biliary atresia, who have a normal gallbladder treon ultrasound. Late congenital syphilis in children older than two can present with more severe features that are frequently tested on boards. Things like gummas, facial dysmorphias like saddle nose deformity and frontal bossing, sabershins, Hutchinson teeth, developmental delay, and hearing and vision concerns.

You’ll want to check a non trepanemal test in these kids, as maternal trepanemal antibodies can persist for over 15 months. Patients with congenital syphilis also receive treatment with penicillin G, 50, 000 units per kilo, frequency determined by their age. Thanks so much for listening, now get out there and practice your sexual histories.

Emily, thank you very much. Hopefully you all found this information helpful and we’ll be able to pick syphilis out of the lineup the next time you encounter it in the emergency department. If you want to learn how to produce a podcast episode, reach out to me, just like Emily did, and we will go through the entire process.

If you’ve got ideas for topics, send them my way. Any feedback that you have is greatly appreciated. Send me an email, leave a comment on the blog, a review on your favorite podcast site, or even a message through social media. And as my 12 year old would remind me to say, subscribe and share. For Pam Currens, the Pediatric Emergency Medicine Podcast, this has been Brad Sobolewski.

See you next time.

Cervical Spine Injuries Jun 05, 2024

Cervical Spine Injuries are fortunately rare in children. this episode is all about learning when to suspect them, how to immobilize the C-spine properly, and which imaging test to choose. It was inspired by a hot-off-the-presses publication from the Pediatric Emergency Care Applied Research Network (PECARN) focused on clinical decision rules for cervical spine imaging in children.

Check out the paper by Leonard et al. entitled “PECARN prediction rule for cervical spine imaging of children presenting to the emergency department with blunt trauma: a multicentre prospective observational study” at Lancet Child & Adolescent Health from Leonard et al here!

Maybe there’s a funky music video that will teach you how to clear the C-spine?

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References

Leonard, J. C., Harding, M., Cook, L. J., Leonard, J. R., Adelgais, K. M., Ahmad, F. A., Browne, L. R., Burger, R. K., Chaudhari, P., Corwin, D. J., Glomb, N. W., Lee, L. K., Owusu-Ansah, S., Riney, L. C., Rogers, A. J., Rubalcava, D. M., Sapien, R. E., Szadkowski, M. A., Tzimenatos, L., Ward, C. E., Yen, K., Kuppermann, N. (2024). PECARN prediction rule for cervical spine imaging of children presenting to the emergency department with blunt trauma: a multicentre prospective observational study. Lancet Child & Adolescent Health. https://doi.org/10.1016/S2352-4642(24)00104-4.

Sasser SM, Hunt RC, Faul M, Sugerman D, Pearson WS, Dulski T, Wald MM, Jurkovich GJ, Newgard CD, Lerner EB; Centers for Disease Control and Prevention (CDC). Guidelines for field triage of injured patients: recommendations of the National Expert Panel on Field Triage, 2011. MMWR Recomm Rep. 2012 Jan 13;61(RR-1):1-20. PMID: 22237112.

Leonard JR, Jaffe DM, Kuppermann N, Olsen CS, Leonard JC; Pediatric Emergency Care Applied Research Network (PECARN) Cervical Spine Study Group. Cervical spine injury patterns in children. Pediatrics. 2014 May;133(5):e1179-88. doi: 10.1542/peds.2013-3505. PMID: 24777222; PMCID: PMC9923608.

Baker C, Kadish H, Schunk JE. Evaluation of pediatric cervical spine injuries. Am J Emerg Med. 1999 May;17(3):230-4. doi: 10.1016/s0735-6757(99)90111-0. PMID: 10337876.

Leonard JC, Browne LR, Ahmad FA, Schwartz H, Wallendorf M, Leonard JR, Lerner EB, Kuppermann N. Cervical Spine Injury Risk Factors in Children With Blunt Trauma. Pediatrics. 2019 Jul;144(1):e20183221. doi: 10.1542/peds.2018-3221. PMID: 31221898; PMCID: PMC6615532.

Leonard JC, Jaffe DM, Olsen CS, Kuppermann N. Age-related differences in factors associated with cervical spine injuries in children. Acad Emerg Med. 2015 Apr;22(4):441-6. doi: 10.1111/acem.12637. Epub 2015 Mar 16. PMID: 25779934.

Leonard JC, Kuppermann N, Olsen C, Babcock-Cimpello L, Brown K, Mahajan P, Adelgais KM, Anders J, Borgialli D, Donoghue A, Hoyle JD Jr, Kim E, Leonard JR, Lillis KA, Nigrovic LE, Powell EC, Rebella G, Reeves SD, Rogers AJ, Stankovic C, Teshome G, Jaffe DM; Pediatric Emergency Care Applied Research Network. Factors associated with cervical spine injury in children after blunt trauma. Ann Emerg Med. 2011 Aug;58(2):145-55. doi: 10.1016/j.annemergmed.2010.08.038. Epub 2010 Oct 29. PMID: 21035905.

Transcript

Note: This transcript was partially completed with the use of the Descript AI

Welcome to PEM Currents, the Pediatric Emergency Medicine Podcast. As always, I’m your host Brad Sobolewski, and this episode is all about cervical spine injuries in children. Now, fortunately, cervical spine injuries in kids are rare. They only happen in about 1- 2 percent of pediatric blunt trauma injuries.

But, In children with cervical spine injuries, at least one in five have permanent neurologic deficits, and serious cervical spine injuries, there’s a 7 percent mortality rate. So severe mechanisms are the scenarios where you are most likely to see a C spine injury in kids. So these are motor vehicle collisions with a patient ejected from the car, motor vehicle collision with death of another occupant, and Intrusion into the patient’s passenger compartment of greater than 12 inches at the roof and or greater than 18 inches at any site. So you got to ask the prehospital personnel about the injury and the crash scene fall of a distance greater than 10 feet or two to three times the child’s height diving into a body of water and an axial load. So force applied to the top of the head and acceleration deceleration Injury of the head.

So you hit your head on a dashboard during a head on collision. A clotheslining force. So that’s caused by a rope, a cable, or another object exerting traction on or striking the neck while the body is in forward motion. And certain sports do have a higher association with cervical spine injuries like football, hockey, wrestling, bicycling, trampoline use or riding ATVs. Infants can get a cervical spine injury during breech delivery or, unfortunately, during non accidental trauma as well. Axial injuries, occiput to C2, are much more commonly seen in children under the age of eight – it’s three quarters of all cervical spine injuries. These are most often due to motor vehicle collisions and falls.

Kids this age are more susceptible because of their big lollipop heads. You know, they have a giant head size related to their body size and they have loose joints and ligaments overall. Their C spine fulcrum is higher at birth, it’s at C2 to C3, as opposed to C5 to C6, which is the usual position in older children and adolescents just through the process of normal growth.

The most common injuries seen in these younger patients are growth plate fractures and ligamentous injuries. It’s particularly difficult to diagnose cervical spine injuries in kids under three because they can’t give you an accurate history and cooperate with the exam. Older children, so older than eight, so middle schoolers and up, have a higher likelihood of injuries in the C3 to C7 range.

This makes up about half of the injuries. And these happen during motor vehicle collisions and sports. You more often will see vertebral body and arch fractures as opposed to the growth plate fractures and ligamentous injuries in the younger children. And overall, C spine injury can occur through a lot of different mechanisms including flexion, extension, vertical compression, rotation, or combination of all of the above.

And though we’re talking about injuries to the vertebra, the cervical spine, spinal cord injuries themselves happen either due to direct compression, or disruption of the cord itself by a fracture, fragment, or a sublux vertebra. Let’s go ahead and pivot to initial management. And we need to suspect cervical spine injuries in any patient with multisystem blunt force trauma.

You want to limit spine motion during your primary survey, the ABCs, or the rapid cardiopulmonary assessment. Someone can hold c spine, and we’ll talk about more about maintaining and clearing the c spine in a little bit. You’ll do jaw thrust alone as an airway maneuver. No head tilt. Orotracheal intubation with video laryngoscopy is ideal.

C spine injuries themselves can impact airway maintenance and or patency. So if you have an unstable injury above C3, you can actually have respiratory paralysis. A lower cervical injury could impact the phrenic nerve. The cervical spinal column injury itself may be associated with airway obstruction from retropharyngeal hemorrhage, edema, or maxillofacial trauma.

You should also consider the possibility of quote unquote spinal shock. This is due to the loss of sympathetic output and vasodilatation. So you could worry about this in a bradycardic and hypotensive patient, but in multisystem trauma hypotension is more likely hemorrhage. than it is spinal shock.

Resuscitate with volume and blood. When evaluating the cervical spine in particular, if you can get details on the mechanism, that’s fantastic. You’ve got some specific injury patterns that you should be on the lookout for. So a patient that has hyperflexion can have a vertebral body wedge fracture and disruption of the posterior elements.

A hyperextension Extension injury will compress the posterior elements and disrupt the anterior longitudinal ligament. This is the hangman’s fracture, the posterior neural arch of C1 or the pedicles of C2. Axial load can cause burst fracture, so someone that dives into a pool. A rotational injury will disrupt the facets.

This is more common in combination with an extension or flexion injury, not just rotation alone. And then there’s the specific Atlanto Axial Rotary Subluxation Pattern. It’s often minor trauma in younger children, where C1 and C2 essentially get stuck on each other in a rotary position, and the kid can’t turn their neck.

Children will have some localized cervical pain, muscle spasm, decreased neck range of motion. They may or may not have neurological symptoms, even if they’ve resolved. These can include paresthesias, numbness, or weakness. The distribution of these neurologic symptoms is really variable, and it can range from involvement of single dermatomes to dramatic neurologic deficits including quadriplegia.

The ability to walk does not completely exclude a C spine injury. And interestingly, even children with no symptoms can have a cervical spine injury. There is a retrospective review of children just before the turn of the millennium that found that even 10 percent of that population with cervical spine injury were initially asymptomatic.

Finally, there are some children that you need to be aware are more predisposed to cervical spine injury than others. And this includes children with Down syndrome, clipple feel, osteogenesis imperfecta, marfans, Ehlers Danlos, chronic steroid use, rickets, and more. When it comes to physical examination of a child with a suspected cervical spine injury, remember, immobilize the c spine, either by hand, so another team member holding inline c spine, or by placing a collar, like an Aspen or Miami.

The ABCs are, as always, incredibly important. An axial injury, occiput to C2, causes abrupt cessation of respiration, so that patient will be apneic. A patient who is hypoventilating may have injuries of the spinal cord at the level of diaphragmatic control, so C3, C4, C5. And hypotension, bradycardia, or temperature instability can result from hemorrhagic and or spinal shock.

When examining the neck, you want to maintain in line stabilization. You have to palpate, but don’t press too hard on the spinous processes for local tenderness, muscle spasm, or obvious deformity. Either start at C7 and work your way up, or find C1 and work your way down. Be deliberate about touching each cervical vertebrae.

Tell younger children to use their words. Yes if it hurts, no if it doesn’t. Don’t shake their head. They always do this. A child with midline cervical tenderness. is more likely to have a cervical spine injury than a child with paraspinous muscular tenderness or spasm. Infants and toddlers who can’t cooperate can actually be cleared without imaging after minor trauma if they have a normal neurologic examination that includes mental status and GCS 15 and no other life threatening injuries.

It’s really hard to know if an 18 month old has C spine pain or not. In my experience, doing a neurologic exam is really difficult in the resuscitation area, especially when a patient is supine and has an immobilized c spine. The overall Glasgow Coma Scale and evaluation of tone, strength, sensation, and reflexes constitutes a complete neurologic exam.

50 percent of all children with cervical spine injuries will have some sort of neurological deficit. And yes, doing a neuro exam is hard, and it takes practice. Part of that is learning ways to get patients to participate when they are uncomfortable or scared. And subtle findings are fortunately most common, but harder to elicit.

An isolated sensory deficit is the most common neurological finding in cervical spine injury. Ipsilateral posterior spinal column and contralateral anterior column are tested via light touch. The anterolateral spinal column is tested with pinprick or pain. The ipsilateral posterior spinal column is tested with position sense, so moving that toe, and dysesthesia will localize to the central cord.

And this is a podcast, so I can’t make you conjure up a table in your head, but I think it is important to remember where some deficits will come from if you have injuries at particular levels. And so if you have an injury at C2 to C3, you may just see apnea. C3 and C4 control the diaphragm, so you want to make sure the patient is spontaneously breathing.

C5 is flexion of the biceps. with the palm up, or supinated. C6 is extension of the wrist. C7 is extension of the elbow. L2 through L4 are extension of the knee. L5 is dorsiflexion of the great toe. And S3 and 4 is rectal tone. So absence of rectal tone is a poor prognostic sign, but it’s also not sensitive for cervical spine injury.

In a child with a GCS of 15 with no active neurological complaints, I would argue that a digital rectal exam is pretty invasive, and just squeezing the buttocks together is probably a good proxy. A child with altered mental status, or decreased responsiveness, or high index of suspicion for cervical spine injury should get a digital rectal examination.

And yes, on board exams! You have these spinal cord injury syndromes. They show up again and again and again. I’ve actually rarely seen them in pediatric practice, fortunately. But for completeness, here they are. Anterior cord syndromes are from hyperflexion, and you’ll see paralysis and loss of pain sensation without loss of light touch or proprioception.

Central cord syndromes are from hyperextension, and you’ll see weakness that is greater in the upper as opposed to the lower extremities, and transient burning sensation of the hands and fingers. Brown Sequard syndrome, which is cord hemisection, will lead to ipsilateral paralysis, loss of proprioception, and loss of light touch, and a contralateral loss of pain and temperature sensation.

And then Horner syndrome is disruption of the sympathetic chain. So you’ll see ipsilateral ptosis, meiosis, and anhydrosis. Okay, so let’s say the ABCs are normal, GCS is 15, and there are no focal neurologic findings. How do we attempt to clear the C spine? So for this, you’re gonna need another team member.

So have the patient lie supine. Have your assistant hold inline C-spine mobilization. They’re gonna be standing above the patient’s head, and then you’ll remove the anterior front portion of the collar. Reach behind their neck, inside the back portion of the collar, and feel very intentionally. See one all the way down to C seven.

Or the reverse, C7 all the way up to C1, asking the patient at each one if there is pain. And again, tell them to use their words, yes or no, and not nod or shake their head. And they’ll still mess this up. At each cervical vertebrae, feel for any swelling or step off. So one that feels kind of more in than the rest.

If there is pain at any cervical vertebrae, replace the collar. And then you’ll move on to imaging, which we’re going to talk about in just a moment. If there is absolutely no pain in C1 through C7, You can have your teammate release inline c spinal mobilization and then ask the patient to actively flex, extend, and rotate to the left and right, all at 45 degrees.

If they have no pain in the midline with any of these movements, then the cervical spine is clinically cleared. But if they have pain or decreased range of motion in any direction, replace the collar and move on to imaging. No matter where you work, you should apply clinical decision rules with an imaging algorithm for anybody with suspected cervical spine injuries.

Now in grown ups, you’re probably familiar with the Canadian C spine rule. It’s a highly sensitive rule that is designed to prevent missing cervical spine injuries while limiting the amount of unnecessary radiologic examinations. This Canadian C spine rule does not apply to children under 16 years of age.

In many settings in adults, plain radiographs have actually been abandoned in favor of CT scans. And a negative CT scan, if you rule in via the Canadian C spine rule, is generally sufficient to clear the majority of C spine injuries and allows for collar removal. In children, though, we prioritize limiting radiation risk.

And so it’s recommended, based on recent evidence from the Pediatric Emergency Care Applied Research Network, PCARD, that we have a three tiered decision rule. So the highest risk patients, these patients have a risk of cervical spine injury of about 12%, are going to recommend immediate medical attention.

CAT scan. These patients will have altered mental status, A GCS of three to eight or unresponsive on the AVPU alert, voice pain, unresponsive, mnemonic. Highest risk patients also include those with any abnormality of the airway, breathing, or circulation. and somebody with a focal neurological deficit. And then there’s an intermediate risk group that has a just under 4%, specifically a 3.

6 percent chance of a cervical spine injury. And these are patients that it is recommended to get a plain x ray. These are patients with posterior neck pain, altered mental status, but a GCS of greater than eight. Or patients with a substantial head or torso injury and substantial means that they’re going to require an intervention or observation in the hospital.

And then there’s a low risk group with a risk of cervical spine injuries of 0. 2 percent or less. And these patients generally don’t need any imaging. And so this is, uh, Assuring through meticulous investigation that none of the following risk factors are present. So neck pain or midline posterior neck tenderness, decreased range of motion or pain with range of motion on flexion, extension, or rotation to the left and right, torticollis, altered mental status so a GCS of 14 or less, any focal neurologic finding and remember sensory deficits are the most common in cervical spine injuries, Any substantial coexisting injuries, so especially torso injuries or child abuse injuries.

Any relevant predisposing condition like Down syndrome. And high risk mechanisms. Diving, hanging, an axial load force, a clothes lining force, or a motor vehicle collision with significant intrusion, ejection from the vehicle, or a death in the vehicle. So again, if the child is negative for all of those, you don’t have to place a collar.

And you don’t need any imaging, and that includes an x ray or a CT scan. The goal of using this high intermediate, low tiered approach is to cut the rate of CAT scans in children by greater than 50%. And so the Pediatric Emergency Care Applied Research Network is actively working on that, initially in an ED setting, with future work in the pre hospital setting.

And so hopefully that helps you understand when to get imaging. But what about the actual imaging choices themselves? Plain x rays are the initial choice in children with normal mental status, but cervical spine tenderness. They’ve got adequate sensitivity to exclude unstable c spine injuries. There are two view x ray series of the neck, that’s an AP and a lateral, or a three view series, cross table lateral, AP, and when obtainable, then open mouthed odontoid.

Multiple views, as you’d expect, are more sensitive, like 90%, as opposed to a single view, which is only 79%. Some children are chunky, and it’s hard to see all seven cervical vertebrae, but you do need to see that for a complete set of film. Some of you might work at a place where they get the swimmer’s view, where they grab both patients hands or wrists, and then pull down to try to get the shoulders out of the way to show C7.

If you have a high suspicion for cervical spine injury, don’t do this. Flexion extension views have fallen out of favor in my practice environment because CT is readily available. The FlexX views are still used in some situations, and they could show some ligamentous disruption. This is where the patient actively flexes and extends with X rays taken.

Never do passive flexion of a suspected C spine injury. CT or CAT scans, by default, get axial images. computed axial tomography. Then the computer is going to do fancy sagittal, coronal, and 3D reconstruction, which is totally cool. CT scans are indicated in any child with altered mental status, a GCS of 3 to 8, or unresponsive on the AFPU.

Also, in children with an abnormal airway breathing and or circulation. and orifocal neurologic deficit. The risk of radiation is the primary concern here, and radiology departments should follow the ALERA, or as low as reasonably acceptable, principle. A C spine CT delivers substantially more radiation to the skin, thyroid, and spinal cord, up to 10 50 percent more.

Children younger than 5 years of age are more prone to radiation induced malignancies due to the increased radio sensitivity of certain organs and a longer latency or life period to develop a cancer. Calculating the lifetime risk of getting cancer from CT scans is hard to do, which is great because we’re not just like scanning people for no reason and seeing if they get cancer later.

The best current estimate is that the estimated lifetime cancer mortality risk attributable to the radiation exposure from a CT for a one year old is approximately 0. 07 to 0. 18%. So not zero, but pretty low. The risk of radiation exposure exceeds the benefit of CT imaging in the majority of children evaluated for C spine injury.

So most of them don’t have a very low GCS, or abnormal ABCs, or focal neurologic deficits. That’s why PCARN is doing this work. Many adult centers will readily get CT scans in adults with suspected c spine injuries. These are just not necessary in the majority of children. Either nothing or plain x rays are sufficient.

And what about MRI? It’s becoming increasingly available. In anybody with an abnormal neurologic examination, or when imaging of the spinal cord or other soft tissues is paramount, MRI can be very helpful. For It is superior to CT for visualizing soft tissues and identifying intervertebral disc herniation, ligamentous injuries, and spinal cord edema, as well as hemorrhage, compression, and transection type injuries.

MRI is actually less sensitive than CT for detection of fractures of the posterior elements of the c spine and injuries to the cranial cervical junction. So it’s not perfect. Even fast protocols for MRIs are tough to get in children under the age of 6 years, they require sedation. And spinal cord injury without radiographic abnormality, C.

Wura, was defined way back in 1982, and I was 4 or 5 years old when this happened. And this was objective signs of myelopathy as a result of trauma in the absence of findings on plane radiographs, flexion extension radiographs, and cervical CT. CWRA is kind of a moot point when you have an imaging modality that uses fancy magnets to jiggle water molecules and take a cool picture.

You can demonstrate injury to the spinal cord and spinal ligaments. And so in anybody with a localizable neurologic sign or symptom, I’m not saying you have to get it in the ED because that’s just not practical, but these patients will, upon admission or shortly after their initial assessment, need an MRI at some point.

And though this episode is focused on cervical spine injuries, it goes without saying that if somebody has thoracic or lumbar spine pain, they should get plain imaging of that, or if they have substantial multisystem trauma and you’re getting a CT scan of the chest or abdomen, that is obviously going to include those bones as well.

Now moving on to disposition. Any patient with a cervical spine injury or a neurologic deficit They’re getting admitted to the hospital. And this obviously includes patients who need surgery, like unstable fractures and those sort of things. That’s a spine or neurosurgery operation. Patients with stable fractures, so an isolated spinous process, or transverse process fractured, identified by CT, will have a rigid cervical collar applied, so an aspen or vista, With trauma and spine follow up within a week.

Kids wear this collar 24 7. So again, you’ve got an isolated, stable fracture, no displacement, no neurologic symptoms, no other injuries, that kid could go home and they’re going to wear that collar 24 7. You have to teach them how to take care of it. If you have a negative x ray, but persistent midline c spine pain, we also recommend keeping the kid in the cervical collar and follow up at a trauma or spine center within a week.

Could you get a CT scan in those situations? Yes, but still most pediatric trauma centers will void the ionizing radiation of the CT scan and keep the patient in the collar until trauma follow up. Okay, so let’s wrap up this episode. Fortunately, cervical spine injuries in children are rare. You should learn how to clinically clear a C spine and know that it takes two people to do it correctly.

Practice your neurologic examination in children who are being evaluated for traumatic injuries. Know which mechanisms are more likely to cause C spine injuries. And make sure that you’re using a clinical decision rule with an imaging algorithm for kids with suspected C spine injuries. Highest risk patients should get CT scans.

They have a 1 in 8 chance of a c spine injury, altered mental status, GCS 3 to 8, unresponsive, abnormal ABCs or focal neurologic deficit. Patients that are intermediate risk have a less than 1 in 25 chance of a c spine injury and that’s when we would get a plain x ray. So they have Posterior midline neck pain, altered mental status, but a GCS of greater than 8, or some substantial comorbid head or thoracic injury that requires management or admission to the hospital.

Patients with no findings will have a less than 0. 2 to 0. 3 percent chance of a cervical spine injury and don’t need any imaging at all. So this is a patient with no midline neck pain, no pain on neck range of motion, Normal mental status, normal neurologic exam, no comorbidities, and no high risk mechanisms.

I encourage you all to take a look at the new publication from the PCAR Network in Lancet Child and Adolescent Health. I’ve provided a link in the show notes. This is the state of the art paper on the use of decision rules for cervical spine imaging in children. To learn more about the Pediatric Emergency Care Applied Research Network, or PCARN, check out PCARN.

org. You can also follow them on x at pkarn team. If you’ve got feedback on this episode, send it my way. Email, direct message on x, a comment on the blog, I’d love to hear it. Hopefully you found this information useful and you can take it back to your next shift. Overall, that’s the goal of this podcast.

Encourage your colleagues to listen and subscribe. Hopefully they will find it helpful as well. And please let me know if there are any topics specifically related to trauma and injuries in children that you think that I should cover. For PEMCurrents, the Pediatric Emergency Medicine Podcast, this has been Brad Sobolewski.

See you next time.

Febrile Seizures May 09, 2024

Febrile Seizures are among the most common neurological problema in young children, occurring in 1 out of 50 children between the ages of 6 months and 5 years of age. This episode of PEM Currents: The Pediatric Emergency Medicine Podcast is a Question and Answer style exploration of some of the most common learning points in this incredibly important topic.

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References

Xixis KL, Samanta D, Smith T, et al. Febrile Seizure. [Updated 2024 Jan 19]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK448123/

Feenstra B, Pasternak B, Geller F, et al. Common variants associated with general and MMR vaccine-related febrile seizures. Nat Genet 2014; 46:1274.

Mullan PC, Levasseur KA, Bajaj L, Nypaver M, Chamberlain JM, Thull-Freedman J, Ostrow O, Jain S. Recommendations for Choosing Wisely in Pediatric Emergency Medicine: Five Opportunities to Improve Value. Ann Emerg Med. 2024 Feb 11:S0196-0644(24)00017-9. doi: 10.1016/j.annemergmed.2024.01.007. Epub ahead of print. PMID: 38349290.

Guedj R, Chappuy H, Titomanlio L, De Pontual L, Biscardi S, Nissack-Obiketeki G, Pellegrino B, Charara O, Angoulvant F, Denis J, Levy C, Cohen R, Loschi S, Leger PL, Carbajal R. Do All Children Who Present With a Complex Febrile Seizure Need a Lumbar Puncture? Ann Emerg Med. 2017 Jul;70(1):52-62.e6. doi: 10.1016/j.annemergmed.2016.11.024. Epub 2017 Mar 2. PMID: 28259480.

Shinnar S, Hesdorffer DC, Nordli DR Jr, Pellock JM, O’Dell C, Lewis DV, Frank LM, Moshé SL, Epstein LG, Marmarou A, Bagiella E; FEBSTAT Study Team. Phenomenology of prolonged febrile seizures: results of the FEBSTAT study. Neurology. 2008 Jul 15;71(3):170-6. doi: 10.1212/01.wnl.0000310774.01185.97. Epub 2008 Jun 4. PMID: 18525033.

Murata S, Okasora K, Tanabe T, Ogino M, Yamazaki S, Oba C, Syabana K, Nomura S, Shirasu A, Inoue K, Kashiwagi M, Tamai H. Acetaminophen and Febrile Seizure Recurrences During the Same Fever Episode. Pediatrics. 2018 Nov;142(5):e20181009. doi: 10.1542/peds.2018-1009. Epub 2018 Oct 8. PMID: 30297499.

Transcript

Note: This transcript was partially completed with the use of the Descript AI

Welcome to PEMCurrents, the Pediatric Emergency Medicine Podcast. As always, I’m your host, Brad Sobolewski. This episode is all about febrile seizures, one of the most common neurological problems that you will see in the emergency department in children. And you know what? I’m going to structure this episode like a bit of a question and answer session.

I’ll ask a question, and then I’ll answer it. So the first and perhaps most important question is, What are febrile seizures and how common are they? Well, they are the most common neurologic disorder of infants and young children, and they happen in about 2 to 4 percent of children between the ages of 6 months and 5 years of age.

I’ll tell parents that they happen in about 1 out of 50 kids. It’s associated with fever, but in a child without evidence of intracranial infection. They are not considered a form of epilepsy. They peak between 12 and 18 months of age, the male to female ratio is 1. 6 to 1, and there is a higher prevalence reported in certain regions like Japan’s Mariana Islands.

A febrile seizure, very simply, is a convulsion associated with a temperature greater than 38 degrees Celsius. The child does not have any acute systemic metabolic problems like hypoglycemia or hyponatremia, and you don’t have to test for those. We’ll talk about that later. And they have no history of previous afebrile seizures.

So why do they happen? Well, they’re likely related to a vulnerability of the developing nervous system to the effects of fever. The neurons that generate these seizures aren’t completely myelinated until age 6. And these neurons that are undermyelinated are more hyper excitable by cytokines during fever in these younger children who get sick more often.

And of course, underlying genetic susceptibility plays a role. And so other risk factors include a high fever, A viral infection, certainly particular viruses. A recent immunization. Hmm. Family history of febrile seizures. Prenatal exposure to nicotine. Atopic diseases. And maybe iron deficiency anemia. And so check this out.

Febrile seizures are due to the degree of fever, not the rate of temperature rise, even though we see them as the temperature is increasing rapidly in the early parts of the illness. And this has been known since the 1950s. The majority of children have febrile seizures on the first day of illness. In some cases, it’s actually their first manifestation of illness.

Like, they’re just a little bit congested, and then they’re convulsing. And then they find out that they’re febrile. The degree of fever associated with febrile seizures is variable, and it depends on the kid’s threshold convulsive temperature. So everybody has a little bit of a different set point. But most often, the fever is greater than 39 degrees Celsius, but 25 percent of febrile seizures do occur between the temperatures of 38 and 39.

In a study of just over 100 children, the temperature of febrile seizures was significantly higher than the mean temperature of fevers in children that did not have seizures, so 104 versus 103. 3. The seizure threshold is lower in infants. who have more febrile illnesses. So viral infections are often associated with high fever in kids, you know that.

One of the most classic viruses associated with febrile seizures is HHV 6. So human herpes virus 6. Another common one is influenza, specifically influenza A. So HHV 6 is the cause in one third of all first time febrile seizures in U. S. children under 2 years of age. The mean maximum fever in infants with a primary HHV 6 infection is generally 39. 5 Celsius, so 103 Fahrenheit or higher. So the incidence of febrile seizures associated with primary HHV 6 infection is estimated as high as 36 percent in 12 to 15 month olds. Other common causes include adenovirus RSV, HSV, CMV, HHV 7, and in Asia, influenza A is number one. The type of viral infection is not important in predicting the future recurrence of febrile seizures or whether or not the child will have a complex febrile seizure.

In kids up to two and a half years of age, breastfeeding may be a preventative factor for febrile seizures. Vaccines don’t cause autism, but they might cause febrile seizures. So the risk of febrile seizures is increased after administration of diphtheria, tetanus, toxoid, and whole cell pertussis, along with measles, mumps, rubella, and MMR with varicella vaccines.

The absolute risk is small, and genetic susceptibility likely plays a role in seizures after vaccines. The risk of a future febrile seizure with a subsequent vaccine is generally lower than the risk of the disease that you are vaccinating against. In drug company sponsored studies, the absolute risk of a febrile seizure after an MMRV vaccine is about 3 to 4 febrile seizures for every 100, 000 children receiving the vaccine.

So again, pretty darn low. So how do we categorize febrile seizures? We all know that there’s simple, That may not be the best terms, but that’s what we’ve got. So the focality, in a simple febrile seizure, they are generalized. A complex febrile seizure is focal, so the shaking is limited to one limb or one side of the body.

The duration, the duration for simple febrile seizures is less than 15 minutes, though 10 minutes has been proposed. Complex febrile seizures, on the other hand, are longer than 15 minutes. A simple febrile seizure is limited to a single episode in a 24 hour period, whereas complex febrile seizures, there is a recurrence of more than once in that 24 hour period.

Overall, 80 percent or more febrile seizures are simple, and 20 percent are complex. Ultimately, though, the history that you get may not be reliable. Both the motor movements and characteristics of the seizure, as well as the duration, are really hard to assess in a patient’s home. Obviously, you should ask about immunization status and whether or not the child has any underlying medical or neurologic problems or developmental delay.

And let’s be honest, the term simple sort of undersells how scary this is for families. There’s nothing simple about watching their child have convulsions and looking like they were gonna die. And why does the complex heterogeneity? Think about it this way. Two one minute seizures occurring an hour apart in a well appearing febrile child seem different than focal one sided convulsions or febrile status epilepticus.

More research is needed. So what’s the recurrence risk after febrile seizures? This is an important thing that we talk to families about. So the overall recurrence rate is approximately 30 to 35%. I will tell parents it’s a one in three chance. If you have two or more febrile seizures, you have a 50% chance of subsequent events.

The subsequent seizure is almost always similar to the first. So 95% of initial simple febrile seizures have recurrent, simple febrile seizures. And interestingly, they’re usually about the same length as well. The risk of recurrence is much higher in children under 12 months of age. So, though it’s one third overall, it’s about 50- 65 percent in children under 12 months of age when they have their first febrile suture.

In older children, like preschool and above, the risk is less than 20 percent. In a study published by Berg in Archives of Pediatrics and Adolescent Medicine in 1997, when I was a freshman in college, they looked prospectively at 428 children with a first febrile seizure. They noted that 17 percent had one recurrence, 9 percent had two recurrences, and 6 percent had three or more.

Three quarters of these recurrences were within one year of the initial seizure, and almost all were within two years. They found four factors for increased recurrence risk. Young age, history of febrile seizures in a first degree relative, lower degree of fever while in the emergency department, and brief duration between the onset of fever and the initial seizure.

Kids with all four of those had a 70 percent risk of recurrence, none of them only 20%. Complex features on the initial seizure were not associated with the risk of recurrence. Other factors that have been reported regarding recurrence in the literature include abnormal development before the first febrile seizure, recurrence of seizures within the same illness, children with one recurrence, and of course children who have had an unprovoked seizure after a febrile seizure are more likely to have future febrile seizures.

So what’s the risk of epilepsy following a febrile seizure? Well, 1% One out of a hundred human beings have epilepsy. If you have one simple febrile seizure, your risk of epilepsy is somewhere between 1 and 1. 5 percent. So it really doesn’t go up significantly. In a normal child with a simple febrile seizure, that risk is only slightly above that of the general population.

So they don’t really need a neurologic workup. Complex febrile seizures or a child with abnormal developmental history, or a child with a family history of epilepsy, have a risk of epilepsy development of about 5 to 10 percent after a febrile seizure. Some other factors related to the risk of epilepsy, if that first seizure is complex, the risk of epilepsy is about 18 times that of simple febrile seizures.

If the child has focal seizures, prolonged seizures, and repeated episodes within 24 hours during the same illness, the risk of epilepsy is 2%, 7%, 20 percent and 50 percent was 3, or all of those risk factors. One cohort study of almost 200 children with febrile seizures found the risk of epilepsy was highest in the first five years and appeared to decrease over time.

And other risk factors for epilepsy that have been identified in independent studies include Todd’s paralysis, short fever duration before the seizure, late onset of febrile seizures over three years of age, and multiple febrile seizure recurrences. There’s a tenfold increase. So what’s the evaluation and management for simple febrile seizures?

I joke that it’s discharge home, but really, Choosing Wisely recommends that we do not order laboratory studies or CT scans for a patient with a simple febrile seizure who has returned to baseline mental status. Labs just aren’t necessary. This postictal period is usually brief, so 20 to 30 minutes or up to 2 hours.

I think 2 hours is too long. And if the kid returns to a neurologic baseline, they’re unlikely to have a metabolic or structural abnormality that you’re going to need to identify. So in that child who has recovered with a normal neurological examination, You don’t need labs. They’re painful, they can give you erroneous or unexpected or irrelevant results, and they’re expensive.

So really focus on targeted testing. If you think they’re at risk for a UTI, well, yeah, get a urine. Go after COVID and flu if you think the swabs are beneficial or strep, but otherwise, you can avoid labs. In general, I think parents are most worried that their child’s gonna have a brain tumor or something wrong inside their head, and naturally, their minds will gravitate towards getting a CT scan.

These are expensive studies with a large amount of radiation, and in the absence of concerning signs on history in the exam, the rate of scarring abnormalities, mass, stroke, or other problems is really, really low, so like less than 1%. So in general, you don’t need a CT scan to show that the brain looks normal.

Children with recurrent febrile seizures or epilepsy following febrile seizures benefit more from MRI and EEG. What about complex febrile seizures? How do we evaluate and manage them? So again, focal onset greater than 15 minutes and or recurrent within 24 hours. The majority of children who develop complex febrile seizures will do so with their first seizure.

Todd’s paresis, so transient hemiparesis following a febrile seizure, usually of a complex or focal type, is rare and happens in about 1. 5 to 2 percent of cases. Prolonged or focal febrile seizures have a higher likelihood of meningitis or structural abnormalities, but still that risk is low. And so even in complex febrile seizures, if the child recovers, EEG or MRI may be the only test, if any, that they need.

You should develop a specific plan for each patient with each patient. A pediatric neurologist. So in terms of lumbar puncture, yes, you can get an LP and CSF studies to exclude meningitis or encephalitis in a child with a complex febrile seizure. The literature has long told us that in children older than 6 months of age who are completely vaccinated, you do not need to get an LP and CSF.

to rule out meningitis in a child with a simple febrile seizure. Admittedly, 25 percent of children with meningitis will have seizures at or before the initial presentation, but almost all of these kids will also have other signs and symptoms of meningitis, like altered consciousness, nuclear rigidity, a petechial rash.

So if you have a child with a complex febrile seizure, but they don’t have any other signs of meningitis, you don’t necessarily need to tap them. If febrile seizures occur after the second day of illness, if you have febrile status epilepticus, these should be other considerations as to whether or not an LP is needed.

But overall, the yield of LP is very low. Now note that pleocytosis can be seen in epileptic seizures, but it’s actually rare in febrile seizures without meningitis. So what does the AAP say? Well, they say that LP should be performed when there are meningeal signs or symptoms or other clinical features that suggest possible meningitis or intracranial infection.

Yeah, you should consider it in infants between 6 and 12 months of age if the immunization status for Hib or strep pneumonia is deficient or undetermined. So, 3, Strep pneumos, and two or three HIBs. And you should also consider an LP when the patient is on antibiotics, because antibiotic treatment could mask the signs and symptoms of meningitis.

This is perhaps the most nuanced scenario. If a child has a complex febrile seizure, and fortunately it’s a rare one that you’ll see, but you should consider, maybe they’re on otitis media, and then they have a febrile seizure, and it’s complex, probably tap that kid. In a study from Kim published in Pediatrics in 2010, they looked at 526 children with complex febrile seizures.

Almost two thirds of this population got lumbar punctures and only three had meningitis, all with a reason to suspect it. So one was clinically non responsive, one had a bulging fontanel and apnea, that’s a bad combo, and one was well appearing but had a positive blood culture for strep pneumonia and they didn’t do an LP, so they just presumed that they have meningitis?

I’m squinting. You can’t see that on the podcast, but that kid probably didn’t have meningitis. Another relatively large cohort of children with complex febrile seizures, published in 2017, showed that the incidence of bacterial meningitis in 839 patients with complex febrile seizures was 0. 7%, and none of them had HSV.

All five of those patients with meningitis had a concerning exam, and four out of five were less than 12 months of age. So, if somebody with a complex febrile seizure is going to have meningitis, there’s going to be other stuff going on. Simple febrile seizures do not require neurology consults or admissions.

They can be discharged home. Previously healthy and developmentally and neurologically normal children with two brief self resolved seizures within a 24 hour period, so technically a complex febrile seizure, can be discharged home with as needed neurology referral if the family and you are comfortable with that plan.

For Febrile status epilepticus, you should stop the seizure with medicines and admit to neurology in the PICU. And complex febrile seizures with focal features, strongly consider admission and always discuss with child neurology. And so briefly, let’s talk about that neurology referral and follow up.

Neurology will often see children in the near term with complex febrile seizures who you felt are safe for discharge but need evaluation. EEG itself is not useful in determining the risk of recurrent febrile seizures. If you’re looking for epilepsy, abnormalities are more likely to be seen on EEG when it’s performed shortly after the seizure, so less than 10 days, and when convulsions are of a longer duration and have focal features.

In children with focal complex febrile seizures, neurology is almost always going to get an MRI as well, and in children under 6, they’re probably going to need general anesthesia to do that. Alright, so what about the management of febrile status epilepticus? So originally this was defined as greater than 30 minutes.

It’s back down to 15 minutes, but there’s a current movement to define status epilepticus as greater than 5 minutes. And 5 minutes is a really long time to watch a kid seize, so I get it. In 1 third of febrile status epilepticus, the actual seizure duration is underestimated in the emergency department.

And the clinical clues that a seizure has ended are often subtle. So a child that is no longer seizing will have closed eyes and deep breathing. If the eyes are persistently open and deviated, even if there’s no limb convulsions or stiffening, they may have ongoing focal seizures. It’s really hard to figure this out.

I’ve also seen kids that are febrile having rigers, or just from a sympathetic surge after a seizure. So, response to painful stimuli, closed eyes, regular breathing. These are all subtle findings along with your vitals like capnography that can help you figure out if that kid is still seizing. In a wonderfully named study called Febstat, which was initially published back in 2008 as a multi center perspective cohort of 119 children one month of five years with febrile status, they noted that the median duration of seizures was 68 minutes.

They were convulsive in all but one child. They were continuous in half and intermittent in the other half. Two thirds of these status. Patients were partial. It was the first febrile seizure for 3 out of 4 children in the study. And HHV 6 was the most common identified infectious etiology. There was also a higher than expected family history of epilepsy in this population.

So if the seizure is going on longer than 5 minutes, start with an IV benzodiazepine if you can. So diazepam or lorazepam. Buckle midazolam or rectal formulations like diastat are alternatives if you don’t have an IV. If that first benzodiazepine doesn’t work, give it again at five minutes. If that doesn’t work five minutes later, give a second line drug.

Generally, levotiracetam or Keppra is the first choice for second line, but you could use fosfenitoin or valproate if you’ve got them. So are febrile seizures associated with an increased risk of mortality? This is very pertinent to familial concerns. Early reports actually suggest that febrile seizures were associated with an increased risk of sudden death later on.

We found that that’s probably not true and that small excess in mortality is really restricted to complex febrile seizures. These patients have pre existing neurologic abnormalities. Those are the ones that are really most at risk. Alright, well what about prescribing preventative medicines or rescue drugs?

I don’t think that children that have a single simple febrile seizure need to be prescribed rectal diastats. But if they’ve had a prolonged febrile seizure, including febrile status epilepticus, or have had multiple febrile seizures, prescribing diazepam rectal gel or midazolam nasal spray in an older child who is an appropriate size could be a good idea.

One dose administered rectally or nasally will not lead to respiratory depression. And so in general, if you’ve got a child that’s at risk for a prolonged future febrile seizure, are good candidates for rescue meds. through a process of shared decision making. Now, you could prevent the risk of subsequent febrile seizures by putting a kid on prophylactic anti epileptic medications.

Most febrile seizures are benign and the side effects of the AEDs generally outweigh the benefits. So you don’t need to put somebody on phenobarbital to stop them from having another febrile seizure. So the use of antipyretics, so acetaminophen, ibuprofen, at the first sign of fever does not prevent a recurrence of febrile seizures in a child that’s had one before.

Morata and colleagues did a single center perspective randomized control trial back in 2018 that noted that regular antipyretics may reduce the recurrence of febrile seizures during the same fever episode, so during that illness. But other studies, including one from Rosenblum back in 2013, which was a meta analysis of three RCTs of acetaminophen, ibuprofen, and diclofenac, starting antipyretics, at the onset of illness could not reduce the rate of recurrent febrile seizures compared with placebo.

Why don’t antipyretics work? Well, they facilitate heat loss, but they don’t inhibit heat production, or lower the threshold convulsive temperature during the initial stage of fever that triggers a seizure. Now, interestingly, phenobarbital can actually treat fever and seizures, but, you know, there’s side effects, so it’s not recommended.

Okay. So is there anything else on the differential? If you’re sure it’s a febrile seizure and you know what you’re doing, generally, you’re right. But, kids can have shaking chills, which are involuntary movements in febrile children that are fine, rhythmic, and oscillatory movements about a joint. They rarely involve the facial or respiratory muscles.

They usually involve both sides of the body simultaneously, and they are not associated with the loss of consciousness, and they are suppressible by touch. So shaking chills can easily be differentiated from fevers. Children with breath holding spells, the cyanotic or pallid types, will sometimes have stiffening or convulsing when they lose consciousness.

And yes, I’ve seen kids with colds and fever who have breath holding spells. And then there’s genetic epilepsy plus febrile seizures, which you are not going to diagnose in the ED. These are autosomal dominant seizures. mutations of sodium and calcium channels that lead to seizures with fever in early childhood that continue beyond six years of age.

And then there’s Dravet syndrome. So, Dravet syndrome is also known as severe myoclonic epilepsy of infancy. It will often resemble complex febrile seizures under one year of age. It’s a de novo mutation, so not inherited, of a voltage gated sodium channel in more than 80 percent of the patients with it.

So that’s why phosphenytoin doesn’t work in Dravet syndrome. And if you’ve heard of Dravet, probably the only thing you remember is that phosphenytoin doesn’t work. And I’ve been told by a wise pediatric neurologist where I work that Any female patient under 12 months of age with complex febrile seizures has Dravet syndrome until proven otherwise.

So that’s one special population with a complex febrile seizure, even two in a 24 hour period that deserves special workup. So let’s end with the last and perhaps most important question. How do we talk to families about febrile seizures? Well remember, they are scared, right? I would acknowledge that this was perhaps the most frightening thing they’ve ever seen their child do.

They are worried that it’s not going to stop and that their child would die. They may have felt helpless, but reinforce what they did right. Maybe they moved their child to the floor in the rescue position, or quickly called 911, or got help. All of these are active decisions that the family made to help their child, even if they could not have prevented the febrile seizure.

Define what a seizure is in ways they’ll understand, including how common febrile seizures are. Again, simple febrile seizures, 1 out of 50 children. Explain how the body protects itself during seizures. So there’s a sympathetic surge leading to increased heart rate. The skin will look pale due to peripheral vasoconstriction and shunting of blood to the core organs.

And when you’re seizing, you will close your glottis, your vocal cords, to prevent from aspiration, which leads to perioral cyanosis. So parents often will recall their child stiff, convulsing, and blue in the face. All of these are physiologic things that we expect during seizures, and I think it’s important to address how those were things that the body did You are certainly going to want to say whether or not the child had a simple or complex febrile seizure, because that will dictate what you do next.

Discuss the recurrence risk and what to do if it happens again, i. e., one third after you’ve had one, 50 50 chance after two or more, and you should always be evaluated by default. Talk about the use of antipyretics and their limited impact on recurrence. So they could reduce the risk during this illness, but they don’t necessarily reduce the risk in a future febrile illness.

And use lab tests, and especially CT scans of the brain judiciously. In a child who has recovered, is back to their baseline, has a normal neurologic exam, and no underlying neurologic problems, they’re unlikely to recover. to have any central nervous system abnormalities seen on imaging, nor any significant metabolic or infectious abnormalities seen on targeted lab testing.

So it’s A OK to not get any studies, but remember, you’re not doing nothing. You’re providing education and reassurance to a worried family. You can do this. If the child has recovered and you think it’s a simple febrile seizure, even if you’ve never seen one before, you’re gonna be right. You They’re that common.

I definitely recommend that you practice your speech or approach to febrile seizures before you go into the room if you haven’t done this before. So find an experienced senior resident, fellow, or attending and review it with them. You want to make sure that you can both give the family useful information.

but also not overwhelm them and anticipate what questions they might have. Well that’s it for this episode focused on febrile cedars. I hope you found it useful and will take the information back with you to your next shift in the emergency department. If you have suggestions for other topics that you’d like me to address in the future, send them my way.

I’ll take an email, a comment on the blog, a message on a social media platform of your choosing. My 12 year old told me that I should remind you to subscribe, and and review. Bottom line is I’m just happy if more people listen because that means more people learn and any feedback you can send in my direction, even if it’s in the form of a review, is very welcome.

For PEM Currents, the Pediatric Emergency Medicine Podcast, this has been Brad Sobolewski. See you next time.

Metabolic Disorders Mar 27, 2024

This episode will help you better prepare for and manage children with inborn errors of metabolism in the Emergency Department. Consider it a supplement to what you remember from Biochemistry and the instructions on the family’s laminated care plan sheet. My special guest podcaster, Emily Groopman, is an actual Pediatric Geneticist in training and we hope that you will find this episode useful.

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Emily Groopman, MD, PhD

Emily Groopman, MD, PhD is a first-year resident in the Combined Pediatrics-Medical Genetics Residency Program at Children’s National Hospital/NIH. She did her MD/PhD at Columbia University, where she investigated the diagnostic utility of exome sequencing for kidney disease. She is a member of the Clinical Genome Resource Inborn Errors of Metabolism (IEM) Clinical Domain Working Group, where as a biocurator she assesses the pathogenicity of variants in IEM-associated genes to facilitate expedited genetic diagnosis for IEMs. She aims to become a physician-scientist in pediatrics and medical genetics, engaging in bench-to-bedside research that utilizes multi-omics-based approaches to provide a molecular diagnosis and support personalized care for individuals with suspected rare genetic diseases and their families. You can contact her via email at egroopman@childrensnational.org.

References

Jeanmonod R, Asuka E, Jeanmonod D. Inborn Errors of Metabolism. [Updated 2023 Jul 17]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK459183/#

Rice GM, Steiner RD. Inborn Errors of Metabolism (Metabolic Disorders). Pediatr Rev. 2016 Jan;37(1):3-15; quiz 16-7, 47. doi: 10.1542/pir.2014-0122. PMID: 26729777.

Burton BK. Inborn errors of metabolism in infancy: a guide to diagnosis. Pediatrics. 1998 Dec;102(6):E69. doi: 10.1542/peds.102.6.e69. PMID: 9832597.

Transcript

Note: This transcript was partially completed with the use of the Descript AI

Welcome to PEM Currents, the Pediatric Emergency Medicine Podcast. As always, I’m your host, Brad Sobolewski, and this episode focuses on the management of children with metabolic disorders who present to the emergency department. I know that this is a subject that makes us all a little bit nervous, and you’re just hoping that the parents have a good laminated sheet to tell you everything that you need to do.

Unfortunately, that’s not always the case. And, let’s face it, there are some great principles that you can apply across metabolic diseases to make sure that you are safely taking care of these children. And you’re thinking, hey! Brad’s not a pediatric medical geneticist. No, I’m not. So I called in a ringer.

Or, well, the ringer called me. So my special guest host on this episode is a trainee in pediatrics and medical genetics. Her name is Emily Groopman, and she’s a current resident at Children’s National Hospital. After doing her MD PhD at Columbia University, where she investigated the genetic diagnosis of kidney disease, she started her residency training with the long term goal of being a physician scientist caring for patients with rare genetic disorders.

She came to me with the idea for this episode based on a recognized need to reinforce key principles in the management of children with inborn errors of metabolism who present to the emergency department. I put a lot more information about Dr. Groopman and how to contact her in the show notes. But now I’m going to pass the mic.

Take it away, Emily.

Inborn errors of metabolism, or IEMs, refer to a diverse group of disorders that result from mutations in genes that are involved in pathways responsible for breaking down nutrients and generating energy. In other words, metabolism. While each of these conditions is individually rare, when considered as a group, they are IEMs occur in approximately 1 in 2, 500 births and can have severe health consequences, including ketoacidosis, cardiac arrhythmias, and encephalopathy.

Therefore understanding these diseases, their presentations and their evaluation is critical for emergency medicine providers. So first, a little bit about their etiology and epidemiology. IEMs are primarily caused, as I mentioned, by mutations in genes involved in metabolism. In other words, genes that include enzymes and other proteins that are involved in breaking down nutrients like carbs, proteins, and fats, and generating energy.

IEMs vary in their inheritance. Most IEMs are inherited in an autosomal recessive manner. Meaning that an individual must inherit two copies of the mutation, so one from each of his or her parents, to be affected. Since an individual must have two copies of the mutation to be affected, the parents and other family members who have one copy, which are known as carriers, will be unaffected.

So, importantly, you may not have a positive family history. Other factors, such as environmental influences, epigenetic changes, the microbiome, and additional genes, may also impact the penetrance of IEMs. In other words, whether or not individuals with a disease causing mutation manifest the associated genetic disease, and also the expressivity.

In other words, which features of the disease individuals with the mutation show for these conditions. Now, newborn screening, or NBS, includes testing newly born infants for certain IEMs.

Since which IEMs are tested for vary state by state, the tests used do not, and the tests do not have perfect sensitivity. And not all IEMs are included on NBS, NBS can miss individuals with IEMs. Therefore, and I want to stress this again, negative results on NBS do not rule out the possibility of IEM.

And it’s always worth considering IEM among children, including among older children and teens, who present with suggestive symptoms. So what’s the pathophysiology of IEMs? Now, IEMs result from disruption of major metabolic processes in our body. And these major metabolic processes include carbohydrate metabolism, protein metabolism, fatty acid oxidation, and glycogen storage.

And together, these processes help store us store nutrients from the food we eat and use it to generate energy. Now, carbs are our body’s preferred source of energy. When we eat, our bodies break down carbohydrates into glucose, which can be used by our cells to generate energy, aka ATP, via cellular respiration.

The glucose that is not immediately used to generate energy is stored in the liver and muscle cells as glycogen. When we’re between meals, in other words, we’re not eating, we’re not fasting, our bodies break down glycogen into glucose so that we can continue to generate the energy our cells need to function.

And altogether, we have enough stored glycogen to last for approximately 24 hours without food. Now, let’s say you fasted for that 24 hours, and at this point your glycogen stores will be depleted. At this point, our bodies have to shift to alternate pathways, first going down the hierarchy of gluconeogenesis, where you can make glucose from amino acids and other non sugar compounds, and then fatty oxidation.

In other words, breaking down fatty acids into the compound acetyl CoA, which can be used to generate energy. Now importantly, fatty oxidation yields ketone bodies. And when the body is in a state that it’s relying primarily on fatty oxidation to generate glucose. You’ll need to get, you’ll accumulate high amounts of ketones leading to ketoacidosis, which is a metabolic emergency.

Now IEMs can disrupt any of these pathways and importantly can have severe health consequences. So what are you going to see? On clinical presentation. Now, first off, realize that most IEMs present with very nonspecific clinical features. You won’t be able to diagnose them on history and physical alone.

And biochemical testing is really needed in most cases to independently diagnose a specific IEM. Therefore, in the ED, the goal is really to recognize the science and symptoms on history and physical exam that are suggestive of metabolic disease. identifying which specific IEM the patient has is part of the later long term evaluation, typically with the help of your friendly geneticist.

It is not the job or the expectation of the EM provider. So what are some of these suggestive clinical features? They include neurologic dysfunction, which is one of the most common that includes things like developmental delay, regression, AKA loss of developmental milestones, hypotonia, encephalopathy, or seizures.

GI symptoms are the second most common, and they include vomiting, food intolerance, food aversion, GERD, refractory to normal antireflux measures, diarrhea, and dehydration. You should also think about IEM in cases where you have failure to thrive, exercise intolerance, or autonomic instability. Now, as I mentioned earlier, since these are autosomal recessive disorders, where you need to have two copies of the mutate, of a mutation to manifest disease, oftentimes family history is negative.

However, sometimes you might hear of siblings or other relatives who had early onset neurologic or GI dysfunction or died early in life, and this can often be attributed to sepsis or sudden infant death syndrome because the symptoms of these overlap with IEMs. You also might see a family history of multiple miscarriages and or constant infinity.

Now typically, IEMs involved in glucose, protein, or fat breakdown, which are, the formal term for them is called intermediary metabolism, will have a short asymptomatic interval. They would kind of like there’s a honeymoon period of days to weeks depending on the IEM after birth. And then they’ll present with acute metabolic decompensation in the neonatal period.

And these neonates typically present looking really, really unwell. So they’re lethargic, they might vomit, they’re hypotonic, hypothermic, they might have fever or seizures. And this is due to buildup of the toxic intermediates of the stalled metabolic pathway. Now the important thing for EM providers to know is that this can mimic the presentation of sepsis.

So you should consider IEM on your differential, especially when the ID workup is negative. And the neonate’s symptoms are refractory to standard measures. In these children, in children, IEMs can present with acute metabolic or neurologic decompensation, like vomiting, coma, or seizures, oftentimes precipitated by episode, things that are metabolically stressful.

So think infection, exercise, or change in diet. Now IEMs involving excretion pathways will generally present with symptoms related to the buildup of the toxic metabolites that cannot be excreted. Now, this, because this gets a lot of buzz, hyperammonemia is a very common feature of a number of different IEMs.

And so it’s important to know its presentation. Hyperammonemia presents with difficulty feeding, lethargy, altered mental status, seizures, vomiting, and vital symptoms of anomalies, most commonly loss of regulation or low core temperature. Now, in contrast, individuals with IEMs that involve pathways for accessing stored energy Can be asymptomatic or well appeared for long periods of time as long as they have a steady supply of energy.

So for instance, in infants who often follow a regular feeding schedule, they can slip under their radar as they’re getting enough energy and in a period in routine forms, and they don’t need to then have any kind of tapping into their stored energy. But again, metabolic GI illness, interrupt other interruptions in feeding schedule, intense exercise.

will result in symptoms. And depending on the specific IEM, these can range from severe metabolic decompensation like hypoglycemia or ketoacidosis, to more subtle features like muscle cramps. So to summarize, consider IEM for neonates with severe unexplained progressive or refractory illness shortly after birth, children who have severe neurologic or GI dysfunction, neglects associated with vomiting.

For metabolic stressors like fever or fasting, and children who are presenting with acidosis or hypoglycemia. Now, what should we do for evaluation and next steps in management? So, again, to reinforce, since IEMs have very specific non specific presentations, the goal in the ER is not to specifically diagnose the IEM.

Rather, it’s recognizing the child in front of you may have an IEM and do what you need to do to acute, for acute stabilization for their associated symptoms. So first, like pretty much many presentations, do ABC, get your PALS as indicated, and get IV access. Next, you want to stop the intake of potentially toxic compounds like protein, fat, glucose, and fructose, and this includes NG or G tube feeds if the child does have them.

Make them NPO and give IV, and give IV fluids with 10 percent dextrose, normal saline, or half normal saline. So D10NS or D10 half NS at one and a half times their maintenance rate. And the goal here is to give glucose, which is that, you know, number one, pure substrate for energy iteration metabolic pathways at a sufficient volume or rate so that this patient does not need to use the other metabolic pathways that might be causing their presentation.

Next, get stat labs, look at metabolic anomalies for blood labs. You want to get some lights, you can get a BMP or CMP glucose, LFT, CRP. CK, urea, and also assess their acid base status, so venous, capillary, or arterial blood gas, and also get COAGs. you want to look at their ammonia and lactate and importantly, if you can, , you want to get a plasma sample for some more sophisticated metabolic tests that can be done later.

So those would be a plasma sample for plasma amino acids, organic acids, acyl carnitine, other compounds, which your friendly geneticist, when you consult them will be incredibly happy you got. Now you also want to get some urine samples. You want to check the color and odor with a urine analysis. Look at the pH, whether there’s glucose, protein, ketones in there.

And you can also store some urine sample for downstream testing. As certain metabolic disorders, you want to look at organic acids in the urine. Now, if you end up needing to get an LP, you can also freeze some extra CSF for downstream testing. Aim for around two to five mils. And then, aside from these tests, There are some additional studies that might be indicated by clinical symptomatology.

So for instance, if they’re having cardiac issues, think about getting an EKG or an echocardiogram. If they’re encephalopathic, you want to consider neural imaging, CT or MRI. And importantly, call a stat genetics consult for further guidance or management. These patients typically do need to be admitted, even if it’s just for monitoring, and if they’re very much deranged in their ABCs, their mental status, they may need to be admitted to the ICU.

So you’ve done your initial workup, nothing’s really conclusive yet, and this patient’s still in the ED. your genetics consult hasn’t responded yet. What should you do? First, continue the glucose infusion. Then, once you get the go ahead from your genetics consult, send samples for specialized metabolic evaluation, including plasma amino acids and acyl carnitines, urine amino acids and organic acids, and whatever else your consult recommends.

Keep an eye on their labs. Again, your consult can give you some helpful tips on the frequency of monitoring, including their lights, glucose, lactate, acid base status, and ammonia. And importantly, if you’re at a referring facility, the most important things are really the basics. So get the ABCs, start D10.

If the patient has a metabolic plan, whether it’s in their electronic medical record and or in their carrier gibbous fans. Follow it. This was made by people who know them very well. If labs are very difficult to get, let’s say the kid’s a difficult stick, at least get a finger stick glucose, get IV access, and start those fluids, D10, either NS or half NS, at one and a half times maintenance.

An obtundate or somnolent child can still tolerate intraosseous access, especially if you put the lidocaine in, 0. 5 mg per kg, max 20 mg. You can use 1 or 2 percent Lido. this video. And really get that access in so you can start those fluids and stabilize the child. Make plans to safely transport the child to a tertiary care after stabilization.

and connect and contact genetics and the accepting ED as soon as you can. Emily, thank you so much. I really appreciate you sharing your knowledge and information and hopefully this was a helpful refresher and primer for the next time that you see a child with a metabolic disorder in the emergency department.

If there’s other topics that you want to hear on the podcast, reach out and let me know. I will take an email. I will take a direct message on X. I will take a comment on Facebook or the blog. If you have the time, leave a review. It helps more people find the show, and therefore more people learn about the care of ill and injured children in the emergency department.

And if you’re like Dr. Groopman, And you’re wondering, Hey, can I record a podcast? The answer is yes, you can. If there’s a topic that you’re interested in learning and teaching about, and it relates to the care of children in the emergency department, send it my way. For PEM Currents, the pediatric emergency medicine podcast.

This has been Brad Sobolewski. See you next time.

Vitamin K Deficient Bleeding (Hemorrhagic disease of the newborn) Feb 22, 2024

Newborn infants need intramuscular injections of Vitamin K in order to produce critical clotting factors. If they don’t get it they can have potentially life threatening bleeding.

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References

American Academy of Pediatrics, Committee on Fetus and Newborn. Controversies Concerning Vitamin K and the Newborn. Pediatrics 2003 July; 112(1):191-2.
Ross, JA, Davies SM. Vitamin K prophylaxis and childhood cancer. Med Pediatr Oncol. 2000 Jun;34(6):434-7.
Cornelissen, M., et al. Prevention of vitamin K deficiency bleeding: efficacy of different multiple oral dose schedules of vitamin K. Eur J Pediatr. 1997 Feb; 156(2):126-30.
Greer, FR, et al. Improving the vitamin K status of breastfeeding infants with maternal vitamin K supplements. Pediatr. 1997 Jan;99(1).
Kher P, Verma RP. Hemorrhagic Disease of Newborn. [Updated 2023 Jun 26]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK558994/#

Transcript

Note: This transcript was partially completed with the use of the Descript AI

Welcome to PEM Currents, the pediatric emergency medicine podcast. As always, I’m your host, Brad Sobolewski. Today, we’re gonna talk about vitamin k deficient bleeding, also known as hemorrhagic disease of the newborn. This is a bleeding disorder that manifests in the first few days to weeks of life after delivery. Under the umbrella are a whole range of hemorrhagic diseases, but the most important is vitamin k deficient bleeding.

I’ll get into why in a moment. Vitamin k itself is a fat soluble vitamin mainly synthesized by gut bacteria. Newborns have minimal vitamin k reserves in a sterile gut. And there’s insufficient placental transfer and breast milk is deficient in vitamin K, so that’s why infants need vitamin K at birth. Without it, they can’t produce clotting factors 2, 7, 9, and 10.

You need all those. In brand newborns, the levels are about 20 percent or less of adult values, but within a month after birth, they arise to within normal limits. Other causes of hemorrhagic disease of the newborn include hereditary clotting factor deficiencies such as hemophilia A or B. And the most common item on the differential, especially for late onset, which we’ll talk about in a moment, is trauma, non accidental or accidental trauma. So why am I covering this topic?

Well, a lot of people out there are actually refusing vitamin k for their newborns. Why? Well, families state that they have concerns about the preservative in the injection, maybe that it could cause autism. It doesn’t. The pain from the injection could be harmful to the infant.

They perceive that the intramuscular vitamin k is a vaccine. It’s not. The dose of intramuscular vitamin K is too high. It isn’t. A potential for adverse reactions to an injection like anaphylaxis.

Anaphylaxis can happen after IV infusion and it’s been rarely reported after I’m injection, like winning the Powerball odds. The injection is perhaps a potential entry for germs, that the intramuscular vitamin K causes cancer. So there was 1 study published in the British Medical Journal in 1990. It raised that concern, suggesting that the risk of cancer was doubled in babies that receive vitamin K after birth. Many studies since then in Europe and the United States have refuted this claim and there is absolutely no association between vitamin k and cancer.

Other concerns about vitamin K include that vitamin K may overwhelm the newborn’s immune system. There’s just a general desire to be natural and perhaps a belief that oral vitamin k prenatally to the mother is more effective, but it isn’t. Furthermore, parents who refuse IM vitamin k tend to refuse other preventative measures, including the Hep B vaccine at birth, prophylaxis against gonococcal ophthalmia, which is really bad, and subsequent routine vaccination. Approximately 1 half of the severe cases of vitamin k deficient bleeding are associated with parental refusal vitamin k during the birth and hospitalization. So hemorrhagic disease of the newborn vitamin k deficient bleeding can be categorized into 3 groups based on the age of onset.

Early occurs within the first 24 hours after birth and it’s generally due to maternal medicines that block vitamin k action. Uh, most commonly, these are anti epileptics like phenytoin, phenobarbital, carbamazepine or primidone. They could also be anticoagulants, coumadin, aspirin or even some antibiotics like cephalosporins. The incidence in infants who have not received vitamin k prophylaxis in parents that are on these medicines could be 6 to 12 percent. Classical vitamin k deficient bleeding happens within 1 week of neonatal life, the second through the seventh day.

With vitamin k, the risk is 0.01 percent. If babies are exclusively breastfed and they don’t get vitamin k at birth, that increases the risks. Late onset is from 8 days up to 6 to 12 months. And this is generally exclusively breastfed babies and babies with diarrhea, cholestasis or malabsorption because vitamin k absorption is dependent on bile. The risk is about 1 in 15000 to 1 in 20000 births.

Most common symptom of late onset is intracranial bleeding with a mortality of 20 to 50 percent and all the associated morbidity of an intracranial hemorrhage. The reason for the increased risk in exclusively breastfed infants, I. E. Even those who don’t get any solids or anything else, is because there’s only marginal levels of vitamin K in breast milk. Other causes of late onset, cystic fibrosis, celiac, chronic diarrhea, alpha 1 antitrypsin deficiency, and forms of hepatitis.

So if you suspect vitamin k deficient bleeding, take a good history. These are some of the points in the history that could lead to you making the diagnosis. So take a history of the drugs that mom was on during pregnancy, especially anticonvulsants. Preterm babies are at a higher risk. Breastfed or bottle fed?

Again, bottle- or formula fed infants are at a lower risk because fortified feedings have higher levels of vitamin K. Where was the delivery? Home delivered infants don’t have access to immediate vitamin k prophylaxis at the same rates that hospitalized infants do. So physical findings that you might see in a patient with vitamin K deficient bleeding include cephalohematoma, intracranial bleeding, intrathoracic bleeding, like hemoptysis or associated respiratory distress, intra abdominal bleeding, so you can see melena, hematemesis, you know, isolated GI bleed. You know, you could also think intussusception and mccals.

Skin, you’ll see petechiae on the mucous membranes. You’ll see hemorrhage or petechiae inside the mouth, on the gums, in the nose, excessive bleeding after circumcision, bleeding from the umbilical cord stump after it’s cut and if the umbilical cord falls off, bleeding from vaccine sites. And I mentioned it before and I’ll say it again, but intracranial bleeding is the worst possible outcome. It’s associated with late onset vitamin k deficient bleeding, and it presents with a floppy baby, lethargy, feeding difficulties, bulging fontanels, poor respiratory effort, altered consciousness, convulsions or pallor. These are sick looking babies.

So in evaluation, you wanna get a CBC. Uh, vitamin k deficient bleeding will have normal platelet levels. Thrombocytopenia actually suggests a maternal immune thrombocytopenia in a newborn. They can make antibodies to platelets which can cross the placenta. Clotting profile, the INR will be greater than 4, because again those factors are needed for proper blood clotting.

The PT will be more than 4 times normal. That’s increased due to decreased activity of factor 7. The PTT will also be increased due to decreased activity of factors 2, 9, and 10. The clotting time will be increased due to clotting factor deficiencies, but fibrinogen levels will remain normal. Protein induced by vitamin k antagonists, PIVCA, I guess.

There’s an estimation you can get a lab on that. Any amount of PIVCA is abnormal and indicates vitamin k deficiency. This disappears around day 5 after the administration of vitamin k, but this lab is not part of the routine ED evaluation. Imaging is targeted at the differential diagnosis in the site of bleeding. So get a chest x-ray or an ultrasound, determine if there’s bleeding in the body cavities, you know, the chest or the abdomen.

Um, CT and MRI are most useful to evaluate for intracranial hemorrhage. So treatment. Uh, vitamin k at birth. I think I mentioned that before. So for an infant that’s greater than 1500 grams, so most of the babies that you’ll be taking care of, 1 milligram I’m Less than 1500 grams, 0.3 mgs per kg up to 0.5 mg per kilogram I’m Intravenous vitamin K is not recommended for prophylaxis in preterm infants.

The form that we now give is vitamin K1, It’s a naturally occurring fat soluble form of vitamin k. So before the introduction of vitamin k 1, long before any of us trained, they used vitamin k 3. K3 was a synthetic water soluble derivative. And in higher doses, it was associated with kernicterus hemolytic anemia and hyperbiliruminemia. So vitamin K1, current version, very safe.

Again, in the US, intramuscular vitamin K at birth is recommended. There are no known toxicity or side effects associated with vitamin K1. Now in some parts of Europe, they’ll do oral regimens at birth, at 2 to 4 weeks, and at 6 to 8 weeks. Uh, they can be weekly or even daily. There’s no licensed oral form for newborns in the US.

Some have given infants the injectable liquid by mouth, but it’s not observed and that’s an unstudied intervention. There’s no safety or efficacy data available on that route of administration. In countries that have gone to oral prophylaxis, failures, even with good compliance, have been reported. Failures have not been reported with routine I’m prophylaxis. So based on the available observational evidence, a single I’m dose of vitamin k appears to be more effective in preventing late onset vitamin k deficient bleeding versus oral regimens.

So maternal dietary changes have little effect overall on vitamin K status of the newborn. There was 1 smaller study that showed that 5 milligrams a day or 800 percent of the recommended daily allowance may raise infant serum levels to near formula fed infants in moms that are breastfeeding. But there’s no FDA approved multivitamin that contains that amount of vitamin K. So if you have a baby with hemorrhagic disease of the newborn, in early and classic forms, the treatment is oral vitamin K, 2 milligrams dose, repeated at 2 to 4 weeks and 6 to 8 weeks. And so again, these are milder forms of bleeding.

All breastfed babies with diarrhea and malabsorption situations require an additional postnatal dose of vitamin K to prevent late onset vitamin K deficient bleeding. For the late form of the disease, oral vitamin K is not as efficacious as parenteral. Hence, the 0.5 to 1 milligram single I’m dose should be administered. A presumptive diagnosis of vitamin k deficient bleeding should be made in an infant presenting with bleeding or neurologic symptoms, and either a prolonged PT and or INR, a history of not receiving vitamin k prophylaxis at birth. You should immediately give them 1 to 2 milligrams IV or sub q.

The vitamin k dose should normalize the coagulation profile within 2 to 3 hours. Infants may need resuscitation with blood products if they’ve lost more than 20 percent of their blood volume. And remember, a newborn can become hypotensive by bleeding enough inside their brain. And also, babies may need 10 to 20 ml per kilo of fresh frozen plasma. I’m going to leave you with a quote from Stanford University and Lucille Packard Children’s Hospital.

So the success of vitamin K prophylaxis has been so dramatic that many practitioners have actually never seen an infant afflicted with hemorrhagic disease of the newborn or vitamin k deficient bleeding. Now, it’s a popular trend in some areas to refuse prophylaxis in an effort to keep things natural for the infant. However, it’s important to keep in mind that the infants most at risk for the classic form of the disease are healthy babies who are exclusively breastfed. So we need to work closely with the parents who refuse vitamin k to help them understand the need for prophylaxis and the severity of the disease. The benefit of using I’m vitamin k injection should be explained to parents.

For those that refuse injection, counseling about the adverse effects of vitamin k deficient bleeding should be explained. The alternate oral dose of 2 milligrams should be recommended in the parents that strictly refuse I’m along with a repetition of that dose at 2 to 4 and then 6 to 8 weeks of age. Alright. So that’s all that I’ve got for this episode on vitamin k deficient bleeding AKA hemorrhagic disease of the newborn. Hopefully, you will feel armed to discuss vitamin k refusal with parents, as well as understand the different forms of the disease, including early, which is related to maternal medicines, classical, which is exclusively breastfed infants who don’t get vitamin k at birth, and the late form, which is the most dire and presents often with intracranial hemorrhage. If you have ideas for other episodes or topics you’d like to suggest, send them my way. I will take your feedback via email, a comment on PEMBLOG, a direct message on a social media platform, a snail mail.

However you wanna get feedback in my direction, let me know. Encourage your colleagues to listen to the podcast as well. More listeners means more learning. And, hey, I know that this can be a tough tough topic to discuss with some parents. I think we’re all better armed to have those conversations if we practice them beforehand.

So hopefully, this episode will prepare you for the next time you meet a newborn whose parents are using vitamin k. For PEM currents, the pediatric emergency medicine podcast, this has been Brad Sobolewski. See you next time.

Cellulitis Jan 17, 2024

This episode will help you recognize cellulitis and even differentiate it from erysipelas which is totally a different thing. You’ll also learn about treatment, whether or not a blood culture is necessary, and a whole lot more!

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References

Chen AE, Carroll KC, Diener-West M, Ross T, Ordun J, Goldstein MA, Kulkarni G, Cantey JB, Siberry GK. Randomized controlled trial of cephalexin versus clindamycin for uncomplicated pediatric skin infections. Pediatrics. 2011 Mar;127(3):e573-80. doi: 10.1542/peds.2010-2053. Epub 2011 Feb 21. PMID: 21339275; PMCID: PMC3387913.

Daniel J. Pallin, William D. Binder, Matthew B. Allen, Molly Lederman, Siddharth Parmar, Michael R. Filbin, David C. Hooper, Carlos A. Camargo, Clinical Trial: Comparative Effectiveness of Cephalexin Plus Trimethoprim-Sulfamethoxazole Versus Cephalexin Alone for Treatment of Uncomplicated Cellulitis: A Randomized Controlled Trial, Clinical Infectious Diseases, Volume 56, Issue 12, 15 June 2013, Pages 1754–1762, https://doi.org/10.1093/cid/cit122

Liu C, Bayer A, Cosgrove SE, et al. Clinical practice guidelines by the infectious diseases society of america for the treatment of methicillin-resistant Staphylococcus aureus infections in adults and children. Clin Infect Dis 2011; 52:e18.

Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America. Clin Infect Dis 2014; 59:e10.

Transcript

Note: This transcript was partially completed with the use of the Descript AI

Welcome to another episode of PEM Currents, the Pediatric Emergency Medicine Podcast. As always, I’m your host, Brad Sobolewski, and today’s episode is all about cellulitis. What is it? Well when a break in the skin occurs, normal skin, flora, and bacteria can enter the subcutaneous tissue, where they do not belong, and they can also invade the lymphatic system.

And although this podcast episode is entitled cellulitis, I’m also going to talk about erysipelas. The two terms are not interchangeable. but both manifest as areas of skin, erythema, edema, and warmth. Cellulitis involves the deeper dermis and subcutaneous fat. Whereas erysipelas involves the upper dermis and there’s a more clear demarcation between the involved and uninvolved tissue.

There’s a fun fact, since the ear doesn’t have deep or dermal tissue, it’s always. ear-a-sipelas. I’ll pause for laughter. Anyway, a skin abscess, which is not the focus of this episode, is a collection of pus deep within the dermis or subcutaneous space. Impetigo, also not included in this episode, is a very superficial infection with that honey crusted drainage. There are also bullous versions. So cellulitis tends to develop in a bit more of an indolent fashion over a few to several days, whereas erys syphilis is more acute. You get systemic symptoms faster, such as fever. Chills, severe malaise, and headache. These can precede the onset of the local skin changes and start just in a matter of hours.

Clinically, for both, you’ll see areas of skin erythema. edema and warmth. You can also see petechiae and hemorrhage, as well as superficial bulla, vesicles, or even echemosis. Sometimes you also see regional lymphangitis or enlargement of the regional lymph nodes. If you’ve got a lot of edema surrounding the hair follicles, you can see some dimpling in the skin.

This creates an orange peel texture appearance, peau d’orange. I hope I pronounced that right. I took Spanish in high school. Anyway, the skin is warm to the touch, it’s uncomfortable, it hurts with movement, and some patients can describe an itchiness or a tight feeling in addition to the pain. You may see fever and other systemic symptoms, and cellulitis and erysipelas, especially in children, are nearly Always unilateral.

Bilateral red limbs? That’s probably something different. Complications that you should be aware of include bacteremia, endocarditis, septic arthritis, or osteomyelitis. Full blown sepsis and toxic shock syndrome. Fortunately, those are rare. So, in general, mild cellulitis has no systemic features in a patient with no significant comorbidities.

Moderate cellulitis has moderate swelling and tenderness with some systemic features like fever or tachycardia. Severe cellulitis has severe swelling and tenderness. really affecting function. It’s a larger body surface area, and you’ve got marked systemic features. So fever or hypothermia, extreme tachycardia, tachypnea, altered consciousness, a very unwell appearance, or even hypotension.

So what causes it? Well, bacteria, and the most common etiology. Staphylococcus aureus is actually an infrequent cause of cellulitis in children. But it can be seen more often in penetrating wounds. Methicillin resistant Staphylococcus aureus classically causes abscess formation. So you won’t really see that as the cause of isolated cellulitis or erysiplas in children.

So how do you make the diagnosis? Well, it’s clinical, right? Look for areas of skin that are erythematous, edematous, warm, and painful. Labs or imaging are not routinely necessary. If you think that there’s an abscess, you can diagnose it clinically by a localized area of induration or fluctuance or use an ultrasound.

Cellulitis can look like a cobblestone street on sonogram. And you should consider whether or not an abscess is present if you see significant induration, so thickening or hardening of the soft tissues, of greater than three centimeters or non uniform induration. The lesion’s been present greater than two to three days and changing or getting worse, and there’s a history of a previous incision and drainage in that patient.

And so do you need labs? Nah, not really. And the vast majority of patients of CBC or other labs will not aid in making the diagnosis of cellulitis. What about blood culture? Every febrile kid with cellulitis needs a blood culture, right? Not so fast, right? A blood culture can cost more than $200-300.

If you’re sending the kid home. Well, you definitely shouldn’t be sending a blood culture because if you’re worried about bacteremia and sepsis, that kid needs to stay in the hospital. And think about the risk of a false positive versus the risk of a true positive. So if the risk of a contaminant culture is greater than the risk of actually catching a bacteria, then don’t send it.

The cost of false positive cultures, repeat visits, length of stay, could be in the thousands of dollars. And so a lot of the previous studies on getting blood cultures were done in the immediate post Haemophilus influenzae B and Prevnar vaccine era. And we do now live in an era where these invasive organisms are fortunately not as big of a concern.

Vaccinate your children, people. But we do deal with MRSA. But still, for mild and moderate cellulitis, MRSA’s not really the etiology. And so even if a kid has a fever, But they look better after a dose of acetaminophen or ibuprofen. You don’t routinely need a blood culture. Now you could even admit a kid for IV antibiotics, maybe they’re dehydrated or they can’t take PO for some reason, without sending a blood culture.

So, admission does not mandate a blood culture. As always, you want to check with your local recommendations and follow algorithms present at your institution. So, what about disposition? So, with prompt identification and treatment with a correct antibiotic, which I’ll get to in a few minutes, patients can see an improvement in their signs and symptoms within about 48 hours.

The treatment failure rate is low, less than 1 out of 7, but probably a bit lower than that, with initial appropriate antibiotic treatment. Overall Cellulitis has a really good treatment prognosis. So when do you want to think about admission to the hospital or short stay unit versus discharge? Right, so you should probably admit a patient to the hospital if they have significant systemic symptoms.

You’re concerned about SIRS or sepsis. Again, fever alone does not necessitate admission. Especially if the kid looks better after antipyretics. If you are concerned that the child may need subsequent or future I& D, like they’re forming a phlegmon, they have a deeper infection, like necrotizing fasciitis, or they need sub sexually consultation, these are probably reasons to admit the patient to the hospital.

Now, some facilities have a short stay unit, like in their emergency department. So, if you don’t meet inpatient admission criteria, you’re likely to improve within 28 hours. Maybe the kid failed initial outpatient treatment with 48 hours of appropriate antibiotics, and they need just a day of IV. They’ve got a rapidly expanding lesion, but it’s probably IND.

The kid has a lot of pain. They can’t tolerate oral antibiotics, or they’re less than six months of age. You know, maybe that’s a patient you observe for just 24 hours in a short stay. And fortunately, cellulitis in children under the age of 2 months of age is rare, but those kids should probably be admitted for IV antibiotics as well, and you should get a blood culture in those situations. One example would be neonatal mastitis, a skin infection of the breast tissue.

Alright, so let’s talk about antibiotics. And generally, your best choice for the majority of children is cephalexin. You’d think because MRSA is everywhere. You want to avoid first generation cephalosporins, but it’s still mostly beta hemolytic strep.

And studies, including Chen et al., showed no difference between cephalexin and clindamycin. And what about length of treatment? Well, for mild cases, five days is probably just as good as ten days. But if you have moderate or severe symptoms, a week and a half is a good idea. You’ll see a lot of places start cephalexin plus clinda, or cephalexin plus trimethoprim sulfamethoxazole.

It’s still often done out in the community. A representative randomized control trial from Palin from 2013 showed that the addition of TrimSulfa did not improve outcomes in a very large cohort that contained lots of children. So the bottom line is, even in patients where you think they might have MRSA nasal carriage?

Monotherapy with cephalexin is fine. So, if you’re doing outpatient treatment or you’re transitioning patient to oral treatment after IV, the first line therapy is oral cephalexin. The dose is 50 mg per kg per day, divided every 8 hours or 3 times a day with a max of 500 mg per dose. If the patient has a true allergy to cephalosporins, you do oral clindamycin, 10 mg per kg per dose, every 8 hours, or 3 times a day, with a max of 1, 800 mg per day, or 600 mg per dose.

If you see treatment failure, that’s another reason to do clinda. So if the kid’s not getting better in 48 to 72 hours on cephalexin, you can do the same dosing of clinda that I just mentioned a moment ago. For inpatient treatment, first line therapy is intravenous cefazolin. So 20mg per kg per dose every 8 hours with a max of 1g per dose.

Cephalosporin allergy, you would use clindamycin. And yes, PO and IV clindamycin are bioavailable. But if you’re admitting somebody, there’s probably a reason that they may not be able to take PO. So if it’s IV, it’s 10mg per kg per dose every 8 hours with a max of 900mg. So it’s higher than the max for PO.

And so again, I will reiterate that 5 days for very mild cellulitis is totally okay. But you could do 10 if that’s what you do locally. Moderate and severe, you need 10 days. Some specific scenarios that you might want to deviate from cephalexin, so if there’s a mammalian bite, some don’t need prophylactic antibiotics, and I’ll admit, There’s no randomized controlled trials of dog bites.

I don’t think the IRB would approve that, but if you are concerned about infection, amoxicillin clavulonate, 22. 5 milligram per kilogram with a max of 875 milligram per dose, oral twice daily. If the kid looks well, And the degree of redness or symptoms is very mild, you could do five days, that’s totally okay.

If the child got an infection in a seawater or freshwater environment, there’s some different organisms like Aeromonas and Vibrio and other things that you want to consider. So you would still start with Cephalexin, but you would add Ciprofloxacin, 10 mg per kg, max 500 mg per dose, twice a day. Or Trimethoprim sulfamethoxazole twice a day with an overall treatment length of 5 to 10 days.

And if you definitely think that it’s methicillin resistant staphylococcus aureus that you’re treating, mild cellulitis, you could do trimethoprim sulfamethoxazole or clindamycin. If you’re sure it is moderate MRSA cellulitis, you could do a trial of oral antibiotics with close follow up or vancomycin IV.

And if they have severe cellulitis, Vancomycin IV, and if you have Staphylococcal Scalded Skin Syndrome, consider adding clindamycin. Switch to oral antibiotics as soon as the patient looks better. And there are some cases of cellulitis where you might need a specific subspecialist. So a general surgeon should be consulted if you have cellulitis of the breast, perianal tissues, perineal tissues, a complex of recurrent pilonidal abscess, Though you could drain these and have them follow up as an outpatient.

Or the cellulitis is just large and complex, or you think it’s going to need drainage in a day or two. ENT should see invasive neck cellulitis, especially with significant symptoms, or you’re concerned that it might be a deeper infection. ophthalmology and or ENT for orbital or periorbital cellulitis, orthopedics for septic arthritis, tenosynovitis or osteomyelitis, and dental or oral maxillofacial surgery for facial cellulitis due to dental infection where the kid might need to be admitted.

All right, so that’s all for this episode on cellulitis. Remember, most cases are mild or moderate, and the child will do incredibly well with oral antibiotic therapy, which should generally be cephalexin. You do not need labs, and especially a blood culture, for the vast majority of children with infections like cellulitis or erysipelas.

A fever does not mean you have to get a blood culture or admit the kid. If they haven’t started antibiotic therapy yet, and they look better after they defer vest with antipyretics, Start oral antibiotic therapy and develop a close follow up plan. Well, I hope this episode is useful. Ultimately, my goal is to deliver succinct evidence based information to help you on your next shift in the ED.

If there’s other topics that you want to hear about, send them my way. I’ll take an email. I’ll take a comment on the blog. I’ll take a direct message on Twitter or X or whatever it’s called. Leave a review on your favorite podcast site. That helps other people find it. And if more people can learn, I’m going to be happy about it.

Encourage your colleagues to listen and subscribe to the podcast. And thank you so much for your time and attention. I know you’re all busy out there. For PEM Currents, the Pediatric Emergency Medicine Podcast, this has been Brad Sobolewski. See you next time.

Laryngomalacia Dec 14, 2023

Laryngomalacia, is the most common cause of infant stridor. Early diagnosis is crucial as it can impact a child’s growth and development. Most infants get better on their own, but those with severe symptoms need surgical interventions like supraglottoplasty. Learn all about diagnosis and management of this common problem in this brief podcast episode.

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@PEMTweets on… sigh “X” (Twitter)

My Instagram

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References

Klinginsmith M, Goldman J. Laryngomalacia. [Updated 2022 Jun 5]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK544266/

Hartl TT, Chadha NK. A systematic review of laryngomalacia and acid reflux. Otolaryngol Head Neck Surg. 2012 Oct;147(4):619-26.

Boogaard R, Huijsmans SH, Pijnenburg MW, Tiddens HA, de Jongste JC, Merkus PJ. Tracheomalacia and bronchomalacia in children: incidence and patient characteristics. Chest. 2005 Nov;128(5):3391-7.

Isaac A, Zhang H, Soon SR, Campbell S, El-Hakim H. A systematic review of the evidence on spontaneous resolution of laryngomalacia and its symptoms. Int J Pediatr Otorhinolaryngol. 2016 Apr;83:78-83.

Transcript

Note: This transcript was partially completed with the use of the Descript AI

Welcome to another episode of PEMCurrents, the pediatric emergency medicine podcast. As always, I’m your host, Brad Sobelewski. Your time is valuable and was mine, and that’s why I release these brief episodes, focus on a single topic, get you in, get you out, teach you something. Today, let’s talk about The most common cause of noisy breathing in newborns and infants, laryngomalacia. You’ve all seen this, or should I say you’ve all heard this, And you will hear the symptoms of stridor and noisy breathing, often positional, and it can impact growth and development.

Now I always thought it was just because airways are small and they’re floppier and therefore noisier, but All infants have small airways and all of their cartilage is soft, so there’s more to the picture. So why does this happen? Well, it could be neurologic function. You could have abnormal tone of the laryngeal nerve. You might have an imbalance of demand supply during inhalation in some infants.

And reflux isn’t a direct cause, but approximately sixty percent of infants with laryngomalacia do also have gastroesophageal acid reflux disease. And we know that reflux can irritate and swell the upper airway, potentially worsening obstructive symptoms. So the incidence is unknown, but it’s probably about one in two to three thousand infants. But it might underestimate it because lots of mild cases don’t actually present clinically, and they’re not diagnosed endoscopically. In the past, we thought there was a male predominance, But it’s equally common in female infants, and black and Hispanic infants may have a higher risk compared with white infants.

Low birth weight has also been suggested to be a contributing factor. So when you’re looking at an infant with possible laryngomalacia, You need a very detailed birth history. So were there any surgical procedures or intubations? Parents need to give you information about breathing difficulties, Especially, noisy breathing or episodes of apnea, noisy breathing that worsens with feeding or while lying down may indicate laryngomalacia. You should also ask detailed questions about feeding habits, weight gain, or if the child’s experiencing failure to thrive.

There are, of course, other causes of noisy breathing in infants that are on the differential. Unilateral vocal cord paralysis Often happens after surgery. So if the kid’s not had surgery, it’s pretty much less likely. Bilateral vocal cord paralysis, which is twice as worse, Prevents with biphasic stridor and may require tracheostomy if respiratory distress is significant. Laryngeal papillomatosis can cause a hoarse cry in upper airway obstruction, and it also appears in infancy.

Subglottic hemangiomas are fortunately rare, but they can cause Torrey Strider. Hemangiomas distributed like a beard are suggestive of this. Subglottic stenosis happens via scarring in the subglottic region due to a previous intubation. So stridor may be present in these infants, but it doesn’t typically change with position. And the child’s history would include a NICU stay and an intubation.

Tracheomalacia and bronchomalacia can coexist with a ringomalacia. Expiratory airway sounds are commonly heard in addition to the stridor, and diagnosis needs scope. We’ll talk more about those in a moment. Vascular ring is a rare cause of airway obstruction in infants, and you’d have feeding difficulties in stridor. The best way to diagnose this is through imaging like CT scans.

And finally, you should always think about foreign body aspiration Even in a child who is not eating solids yet. Remember, an older sibling could feed them something. I have seen this before. So an infant is in respiratory distress after being accompanied or the symptoms are persistent, you should always think about a foreign body, especially in the acute setting. The physical exam of a Child with possible laryngeal malaysia focuses on the airway and breathing naturally.

Make sure that the nasal passages are patent. You don’t wanna miss The oral cavity should be explored for cleft lip, cleft palate, glossoptosis, Pierre Robin sequence, or micronathia. Obviously, all of those facial and oral abnormalities can contribute to breathing and feeding difficulties. You wanna check out the neck for masses or vascular lesions. And many infants have hemangiomas, but I mentioned this before.

If you see them in a beard like distribution, worry about airway hemangiomas. So if you have an infant that has some intermittent, noisy breathing on inspiration, and sometimes it’s worse with feeding and when they lay down, you should really think about laryngomalacia. And if the infant is thriving and growing well, not having any apnea or color change, you can kinda wait it out. But if you wanna make the diagnosis definitively, you will need to have an otolaryngologist perform an awake, Flexible fiber optic laryngoscopy. That’s the primary diagnostic tool for infant stridor in general.

You get a comprehensive view of the oropharynx, the supraglottis, the glottis, the subglottic area, and the hypopharynx. For infants with laryngomalacia on scope will have some specific anatomical abnormalities. They’ll have shortened aryepiglottic folds, An omega shaped epiglottis and or redundant arytenoid tissue. And again, The awake flexible fiber optic laryngoscope is the gold standard for diagnosing laryngomalacia. The Kid is awake and breathing, and that allows you to assess the dynamic collapse of the supraglatic airway during respiration.

In the child with more severe symptoms or you’re worried about tracheomalacia, direct laryngoscopy including a diagnostic bronchoscopy in the OR under general anesthesia may provide a more comprehensive look at the Airway and the upper aerodigestive tract. So you’ll scope down to the main stem bronchi in this standpoint. Sometimes you get A triple scope, which is flexible laryngoscopy, bronchoscopy, and upper endoscopy. So three endoscopists together. I don’t know if there’s a discount.

And this is important when there’s severe symptoms or you have concern about synchronous airway lesions. Direct laryngoscopy can also be a prelude to surgical intervention if you need it. Speech therapists could be particularly valuable If there’s issues with swallowing or feeding, if you’re concerned about aspiration or swallowing deficits sometimes they’ll do a modified barium swallow study. Sleep studies can be particularly helpful to look at symptoms of obstructive sleep apnea, especially in older symptomatic infants. As I’ve alluded to before, fortunately, most children resolve on their own by about twelve to eighteen months of age.

So this management is conservative, includes upright feeding, antireflux therapy, so alterations to how you Feed, burp, and position. And no study has yet shown that proton pump inhibitors improve laryngomalacia symptoms, but they’re still widely used. What’s important to remember is that the majority of infants don’t need any intervention. However, there is a small proportion of infants that do have more severe symptoms, like poor weight gain, Feeding difficulties, obstructive sleep apnea, severe breathing symptoms, they’ll need a procedure called supraglottoplasty. And so how is that done?

Well, they could use lasers or cold steel or microdebridement, and it’s really tailored to the individual patient’s anatomy. So you could divide shortened area epiglottic folds. You can remove some redundant arytenoid mucosal tissue. You could do an epiglottopexy or a combination of some of these. And you really obviously don’t wanna scar the infant’s airway or cause glottic stenosis.

Supraglottoplasty is highly effective. Ninety five percent do great and see measurable and significant improvement in their laryngomalacia symptoms. Only about five percent need some sort of provision, And a higher risk of that is seen in patients that were under two months of age when they got the initial procedure or have neurologic or cardiac comorbidities. Neurologic comorbidities have the highest rate of revision surgery. Maybe up to three out of five patients will need a trach due to ongoing airway obstruction.

Aspiration after supraglottoplasty is the main risk, but it’s rare and not significantly associated with the procedure Self. And let’s not forget the main reason that most of you have heard of larynga Malaysia. It’s because a parent was worried about it. It can be scary to have a baby who is breathing noisily. The fear in the back of your head is that the baby could stop breathing and die.

It’s real. I’ve heard it personally. Ultimately, providing reassurance, guidance, close follow-up, and helping the parent understand what they’re doing well can go a long way into making sure that you’re not missing anything else and you’re appropriately monitoring the infant with potential laryngomalacia. Refer to ENT if you’re unsure of the diagnosis or if you feel that it will benefit the patient. It may seem a little barbaric, but an awake Bedside fiber optic scope isn’t actually that big of a deal.

Alright. So here’s some summary points. The majority of patients with Laryngomalacia will outgrow it by twelve to eighteen months. Diagnosis can be suspected clinically, but awake fiber optic Flexible laryngoscopy is definitive. Severe symptoms should be monitored and include recurrent cyanosis or respiratory distress, Apnea and failure to thrive.

These need further workup, including many times direct laryngoscopy and bronchoscopy to rule out other airway abnormalities. Surgery is generally only indicated in patients with severe laryngomalacia, and it’s called Supraglottoplasty. It’s generally well tolerated to highly effective. Patients with neurologic comorbidities or congenital cardiac disease and those less than two months of age are more likely to require revision surgery for relief of ongoing symptoms. Alright.

So that’s it for this episode. Hopefully, you learned something new about laryngomalacia. If you have any other suggestions for topics, send them my way. I’ll take emails, comments on the blog, direct messages on x or Twitter, threads, Facebook, whatever channels you wanna use. My goal is to make sure that you are ready for your next ED shift with up to date information that’s evidence based and ready to deliver to patients and families.

If you have the time, leave a review on your favorite podcast site. That helps with discovery so that more people can listen and learn. And share this episode in the show with your colleagues. I’d love to hear what they think as well. For PEM currents, the pediatric emergency medicine podcast, this has been Brad Sobolewski.

See you next time.

Meckel Diverticulum Nov 28, 2023

Meckel diverticulum is a congenital anomaly of the small intestine that can present with various clinical manifestations, including rectal bleeding and obstruction. Recognizing the characteristic features and understanding the differential diagnosis is crucial in managing patients with lower gastrointestinal bleeding. This episode will help you recognize and diagnose this surgical condition that you probably remember because the “rule of twos.”

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My Instagram

My Mastodon account @bradsobo

References

Dixon P & Nolan D. The Diagnosis of Meckel’s Diverticulum: A Continuing Challenge. Clin Radiol. 1987;38(6):615-9

Ghahremani G. Radiology of Meckel’s Diverticulum. Crit Rev Diagn Imaging. 1986;26(1):1-43

Weerakkody Y, Ranchod A, Yap J, et al. Meckel diverticulum. Reference article, Radiopaedia.org (Accessed on 26 Oct 2023) https://doi.org/10.53347/rID-17174

Sagar J, Kumar V, Shah DK. Meckel’s diverticulum: a systematic review. J R Soc Med. 2006 Oct;99(10):501-5.

An J, Zabbo CP. Meckel Diverticulum. [Updated 2023 Jan 30]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK499960/#

Transcript

Note: This transcript was partially completed with the use of the Descript AI

Welcome to PEMCurrents: The Pediatric Emergency Medicine Podcast. As always, I’m your host, Brad Sobolewski. Your time is valuable and so is mine. And that’s why I release these brief, succinct episodes focused on a single clinical topic, get you in, get you out, teach you something. Today I’m going to talk about Meckel diverticulum. If you haven’t seen it clinically, you have seen it on a test and it is absolutely something that you should be thinking about when you see a patient with bloody stools in the emergency department.

So Meckel diverticulum is a congenital abnormality of the small intestine and it’s the most common cause of significant lower GI bleeding in children. It arises from an incomplete involution of the vitelline duct during embryonic development. You didn’t think I’d say that during this podcast.

Typically occurring during the seventh week of gestation. It’s characterized by a blind ending true diverticulum, a pouch, that contains all of the layers typically found in the ileum. So especially relevant to board exams, Meckel diverticulum follows the rule of twos. So it affects approximately 2 percent of the population.

It’s located about two feet from the ileocecal valve. It’s usually about two inches long. Only about 2 percent of cases actually become symptomatic. It is most commonly diagnosed by the age of two years, with 45 percent of symptomatic cases occurring in this age group. It is two times as common in boys, and there are two types of epithelium found in the meckle diverticulum, gastric and pancreatic.

So the clinical presentation of Meckel can vary depending on the complications that arise. The most common presentation in children Under the age of five years is rectal bleeding, which may be intermittent or just massive, but the bleeding is usually painless. Other complications include obstruction due to intussusception or volvulus, which can lead to bowel ischemia or shock.

Diverticulitis and umbilical fistula can also occur, but that might typically be seen later in life. In approximately a third of cases, Meckel diverticulum may perforate, and traumatic rupture of one could actually occur following blunt trauma. Let’s move briefly into the differential diagnosis of GI bleeding in children.

So, upper GI bleeding is typically not bright red. Now you could have a briskly bleeding ulcer and a liver transplant patient, but that’s not something we typically see in pediatrics. So generally lower GI bleeding is bright red, hematochezia, whereas the upper GI bleeding is maroon or dark black, diverticular disease.

which is rare in children, could cause bright red bleeding. A vascular ectasia or angio dysplasia, which is really hard to diagnose unless you’re an endoscopist. You could have bright red blood from inflammatory bowel disease, infectious colitis, mesenteric ischemia or ischemic colitis, colorectal cancer or polyps, hemorrhoids, both internal and external.

Aortoenteric fistula, or vascular fistulas, which are pretty darn rare in children, and generally a complication of inflammatory bowel disease or previous surgery, a rectal foreign body, a rectal ulcer, which is often associated with HIV, syphilis, or other sexually transmitted infections, or an anal fissure.

So all of these things are on the differential for lower GI bleeding. It’s important to note that if you see diarrhea with blood, as opposed to just frank blood, you should be thinking about infectious problems, like STEC causing organisms, like E. coli 0157:H7 which can lead to hemolytic uremic syndrome, or inflammatory bowel disease, or other problems.

So the diagnosis of Meckel diverticulum is called a meckle scan. I wonder how it got its name. It’s a technetium 99 pertectinate scan, and it’s the classic test of choice for diagnosis. It’s a nuclear medicine study, and the radioactive tracer is taken up by the gastric mucosa, which is in the Meckel diverticulum.

Therefore, it’ll show up on the radiology picture. The sensitivity is reported to be about 60 percent in adults, but 85 90 percent in children. The uptake of the dye can be increased by giving cimetidine or glucagon. So the feeding artery of the Meckel diverticulum is an anomalous branch of the superior mesenteric artery.

It has a long and non branching course and it ends generally towards the right lower quadrant. So the MEKL scan will help you pick up where that gastric mucosa is and then the surgeons can figure out how the blood supply gets there. Ultrasound and CT are not really good at differentiating a Meckel diverticulum from normal bowel.

So, if you think that somebody has a Meckel diverticulum, Here are some following management steps. If the patient has signs of obstruction, insert a nasogastric tube for GI decompression. Give broad spectrum antibiotics to cover potential bacterial infection, especially if the patient is ill appearing.

Give IV fluids packed red blood cells to resuscitate. A CBC and type and screen are great lamps to get. If there’s brisk bleeding or the patient’s unstable, consider COAGs. And yeah, you’re gonna want to consult a surgeon because that is how you deal with asymptomatic Meckel diverticulum. So if you’ve got complications such as significant bleeding, bowel obstruction or perforation, emergent surgical removal is warranted.

This can be done via a laparoscopic or open approach. So I’m going to wrap this up here. Again, this is a brief episode. A Meckle diverticulum is a congenital anomaly of the small intestine that can present with various clinical manifestations, including rectal bleeding. and bowel obstruction. Recognizing the characteristic features and understanding the differential diagnosis is crucial in managing patients with lower GI bleeding.

The Meckel scan is the preferred diagnostic modality. It’s a nuclear medicine scan and prompt surgical consultation is necessary for symptomatic cases. All right, so that’s it for this brief episode. If there’s other topics you want to see me tackle, send them my way. I’ll take your suggestions via email. Direct message on X or Twitter, Facebook, Instagram, telepathy. Any feedback is good feedback. Until next time, for PEMCurrents: The Pediatric Emergency Medicine Podcast, this has been Brad Sobolewski. See you later.

Respiratory viral panels Sep 26, 2023

Just because you can test for dozens of viruses with a single swab should you? Is this actually measuring a current infection, or a recent virus from which the child has since recovered. And what about the cost? Are these tests expensive (spoiler alert: They are!). Learn about the situations when we should get these […]

Constipation: Diagnosis, X-Rays, and more Sep 19, 2023

Where else is the poop going to be? Constipation is by and large a clinical diagnosis. This episode reviews how to make the diagnosis, red flags, and why X-Rays don’t necessarily help assess stool burden adequately in most children. This podcast episode is designed to disseminate the important work of Choosing Wisely, an initiative of the […]

Do we need labs or a head CT after simple febrile or unprovoked seizures? Sep 12, 2023

Labs or CT scans are not necessary to provide additional diagnostic information or reassurance for most children who recover completely following simple febrile seizures or unprovoked first time generalized seizures. The rate of abnormalities on these studies is very low, and the cost and downsides are too high to justify ordering them on a regular […]

Do we need labs to medically clear a patient for psych admission? Sep 05, 2023

For most children requiring admission to an inpatient psychiatric facility laboratory studies are generally not required. Many of the children and adolescents being admitted already have an established mental or behavioral diagnosis, and a reassuring history and exam. The heterogeneity of clinical settings makes it challenging to establish processes that account for the needs of […]

Do children with bronchiolitis, croup, asthma, or first-time wheezing need a Chest X-Ray? Aug 29, 2023

For most children with children with bronchiolitis, croup, asthma, or first-time wheezing chest X-Rays are not necessary. These X-Rays are often obtained due to the possibility of missing pneumonia. But, these radiographs are hard to interpret, increase length of stay and the cost of care, and expose children to excess radiation. This podcast episode is […]

Henoch–Schönlein Purpura (HSP) Aug 08, 2023

Henoch–Schönlein Purpura (HSP) is a common vasculitis seen in younger children. The classic skin finding is palpable purpura in gravity dependent areas of the body (buttocks and legs). Children can also have arthralgias, abdominal pain and intussusception, and even nephritis. Learn about the diagnosis and management of Henoch–Schönlein Purpura (HSP) in this brief podcast episode. PEMBlog @PEMTweets […]

Stings and Envenomations Jun 27, 2023

It is summertime, so the bees and bugs are out! In this episode, Dr. Ben Grebber, a pediatric resident at Boston Children’s Hospital/Tufts Children’s Hospital, discusses Bee Stings and Spider Bites. A very common pediatric summer complaint in emergency departments, urgent cares, and primary care offices, this episode covers common signs and symptoms, some pathophysiology, […]

Agitation Episode 5: The boarded ED patient Jun 14, 2023

We are in the midst of a staggering mental health crisis. Thousands of children and adolescents spend days at time in Emergency Departments waiting for definitive mental health disposition. This podcast episode hosted by Brad Sobolewski (@PEMTweets) and co-authored by Dennis Ren (@DennisRenMD) is all about what we should consider when boarding children in the […]

Agitation Episode 4: Safe prehospital transport Jun 07, 2023

There are protocols in place that assist highly trained Emergency Medical Service providers in assuring that agitated children are safely transported to their destination. This podcast episode hosted by Brad Sobolewski (@PEMTweets) and co-authored by Dennis Ren (@DennisRenMD) is all about what pre-hospital providers should do to get these agitated children safely to the ED. […]

Agitation Episode 3: Pharmacologic management May 31, 2023

When we think of managing agitated patients we think of medicines – but that shouldn’t be our first option. However, medications can be adjuncts to non-pharmacologic means to help keep agitated children safe from harm. This podcast episode hosted by Brad Sobolewski (@PEMTweets) and co-authored by Dennis Ren (@DennisRenMD) is all about age-appropriate pharmacologic management […]

Agitation Episode 2: Non-pharmacologic management May 24, 2023

Agitated children should always be treated with dignity and respect. This entails utilizing the least invasive non-pharmacologic means of assisting them, before moving to physical or chemical restraints. This podcast episode hosted by Brad Sobolewski (@PEMTweets) and co-authored by Dennis Ren (@DennisRenMD) is all about age-appropriate non pharmacologic management strategies for agitated children. It is […]

Agitation Episode 1: Differentiating organic versus psychiatric May 17, 2023

Most children who present to Pediatric Emergency Departments these days with mental health concerns – including agitation – have a known psychiatric problem or diagnosis. Furthermore, the connection between physical and functional symptoms is inextricably linked in many patients. Why then do we persist with the “is it medical/organic or psych” question? Ultimately, this episode […]

Gun Violence and Safety (2023) Apr 26, 2023

Dr. Kit Carney and Dr. Kristen Humphrey discuss gun violence, its impact on our patients and their families, as well as practical tips on advocating for safe storage of firearms, and how we can support victims of violence.

Epiglottitis Apr 12, 2023

The epiglottis is the toilet seat of the airway. That’s a useful function. But what if becomes so swollen and inflamed that it leads to airway obstruction and respiratory failure. That’s bad. That’s also what epiglottitis is. You can also call it supraglottitis. Either way you need to recognize this potentially life threatening malady and […]

Norovirus Feb 28, 2023

Norovirus is the leading cause of viral gastroenteritis worldwide and is also a major cause of food borne illness. It spreads rapidly and causes vomiting and diarrhea that lead to many ED visits. Hopefully this brief episode will enrich the discussions that you have with patients and their families when making the diagnosis of viral […]

Agitation in Neurodivergent Children Jan 24, 2023

“Neurodivergent” is a term used to describe brain functionality and how it differs in some people. These individuals perceive, interpret and interact with the world in ways that are different than what we typically encounter. The Emergency Department is a potentially challenging and stressful place for Neurodivergent children, and this episode discusses strategies to help […]

Commotio Cordis Jan 06, 2023

Commotio cordis is caused by the blunt impact of a hard object directly over the heart occurring during a specific window of ventricular repolarization leading to immediate collapse, ventricular fibrillation, and cardiac arrest. This episode focuses on risk factors and management of this rare but catastrophic injury. PEMBlog @PEMTweets on Twitter My Mastodon account @bradsobo […]

Peritonsillar Abscesses Dec 08, 2022

Peritonsillar Abscesses are the most common deep neck infection in adolescents and young adults. You will see them in grade schoolers as well. Learn about the diagnosis and management, including making the choice between needle aspiration versus wielding a scalpel for incision and drainage. PEMBlog @PEMTweets on Twitter My Mastodon account @bradsobo References Ungkanont K, […]

Tongue Lacerations Dec 01, 2022

Tongue lacerations are surprisingly common in the Emergency Department. Fortunately most of them don’t require any specific interventions. You just let them go and they heal on their own. Really. But if you do have to repair I offer advice in this brief episode. PEMBlog @PEMTweets on Twitter My Mastodon account @bradsobo Resource from the […]

Periorbital Cellulitis Oct 27, 2022

Perioribital cellulitis (AKA Preseptal cellulitis)is a soft tissue infection of the eyelids and skin anterior to the orbit. It must be differentiated from the more invasive and dangerous orbital cellulitis. Treatment varies depending on the original source (sinusitis, local trauma, stye etc,.). Learn all about periorbital cellulitis in this brief episode of PEM Currents: The […]

Neutropenic enterocolitis Sep 28, 2022

Bad things happen when you don’t have enough neutrophils. After getting cytotoxic chemotherapy you tend to have even fewer neutrophils. This can put you at risk for neutropenic enterocolitis which should be suspected in an immunocompromised child with fever and abdominal symptoms. Treatment is broad spectrum antibiotics and the imaging test of choice is CT […]

Chicken Pox Aug 11, 2022

Dewdrops on a rose petal. You’ve all heard the description, right? But how many of you have actually seen chicken pox in the wild. And what about monkey pox – does it look the same? How can I tell them apart? I wish there was a brief podcast episode focused on varicella that would help […]

Hand, Foot, & Mouth Disease Jul 19, 2022

Hand, Foot, and Mouth (and Butt) disease is incredibly popular in the summer/warm weather months in the Northern Hemisphere (August through October). It is so popular that I guarantee you will see it many times. This brief episode will teach you how to make the diagnosis and review strategies for management – which are largely […]

Pain management for laceration repair in children Jun 21, 2022

Laceration repair is one of the quintessential procedures that children undergo in Emergency Departments. Minimizing pain and anxiety for children is a much better idea than just holding them down and getting it done. This episode will teach you all about local anesthetics, when to use anxiolytics and procedural sedations s well as the considerable […]

Lyme Disease Jun 02, 2022

Update 6/6/22 – there is ongoing work to determine the optimal treatment for meningitis in Lyme between doxy and ceftriaxone. The original episode recording did not make this clear – my apologies. The 2021 IDSA guideline suggests that you could use either agent. This episode was edited to reflect this change. Lyme disease prevalence continues to rise […]

Toxic Shock Syndrome May 11, 2022

Toxic Shock Syndrome can be hard to recognize and differentiate from clinical entities such as Kawasaki, MIS-C, and DRESS. This brief podcast episode will raise awareness of situations in which TSS can occur and drive home important management pearls – like why you need to add Clindamycin. PEMBlog.com Follow @PEMTweets on Twitter Check out the […]

Toxicology Season 3 Episode 3: Iron Apr 26, 2022

Iron ingestions always show up on standardized tests and are definitely one of those “many kids are fine but some aren’t and it’s hard to figure out who’s fine and who isn’t” ingestions. Suzan Mazor from Seattle Children’s helps iron out the details… PEMBlog.com Follow me on Twitter @PEMTweets Check out the Facebook page CME […]

Toxicology Season 3 Episode 2: Calcium Channel Blockers Apr 19, 2022

Now this is a frightening ingestion! Calcium channel blockers are hard to manage with refractory shock being one of my main “please don’t let this come to the ED” nightmares. Suzan Mazor breaks it all down and discusses management of this challenging ingestion. PEMBlog.com Follow me on Twitter @PEMTweets Check out the Facebook page CME […]

Toxicology Season 3 Episode 1: Bupropion Apr 12, 2022

There are some scary ingestions out there and I think we’d all agree that bupropion (Wellbutrin) is on the short list of drugs that should make us worry. Learn how to recognize and manage toxicity, especially the neurogenic and cardiac effects of bupropion in the first episode of the third season of Toxicology podcasts from […]

Ultrasound for Appendicitis Mar 25, 2022

This episode of PEM Currents: The Pediatric Emergency Medicine podcast is focused on the use of ultrasound to make the diagnosis of acute appendicitis. You’ll learn about how a right lower quadrant ultrasound is performed, what we look for on the images, how to interpret positive, negative, and intermediate/equivocal results and much more! This episode […]

Nosebleeds Mar 09, 2022

You will see a child with a nosebleed in the ED. It is a mathematical certainty. Chances are it has already stopped. Even if it hasn’t you can stop it – and figure out why it happened – and provide reassurance and education to the patient and family. Yes, all of those things for one […]

Intussusception Feb 11, 2022

Any list of “Top 10 Emergency Department diagnoses in children you can’t miss” should include intussusception. This episode reviews the diagnosis and management in practical manner that should help you on your next shift. It also features the talents of Kriti Gupta, MD, a Pediatric Emergency Medicine fellow from NewYork Presbyterian Brooklyn Methodist Hospital who […]

Urinary retention Jan 19, 2022

This episode of PEM Currents: The Pediatric Emergency Medicine Podcast is a brief review of the management of urinary retention in children. The most common causes are UTI and constipation – but you must be aware of neurological problems and assure that you history is thorough and your physical exam complete. PEMBlog.com Follow @PEMTweets on […]

DVT Nov 19, 2021

Your time is valuable and so is mine. That’s why I’m sharing brief, focused podcast episodes that will hone in on a single problem. This time, it’s deep venous thromboses (DVT). Learn how to suspect them in the first place and make the diagnosis. PEMBlog.com Follow @PEMTweets on Twitter Check out the Facebook page I am […]

Stress Dose Steroids Nov 09, 2021

Your time is valuable and so is mine. That’s why I’m sharing brief, focused podcast episodes that will hone in on a single problem. This time, it’s stress dose steroids. Learn about how to give them and to not worry about tons of body surface area related math when you have a sick child in front […]

Ovarian Torsion Nov 03, 2021

Your time is valuable and so is mine. That’s why I’m sharing brief, focused podcast episodes that will hone in on a single problem. This time, it’s ovarian torsion. Learn about the presentation, diagnosis, and treatment of this can’t miss surgical condition. PEMBlog.com Follow @PEMTweets on Twitter Check out the Facebook page I am proud to […]

Cannabis Hyperemesis Syndrome Oct 29, 2021

Your time is valuable and so is mine. That’s why I’m sharing brief, focused podcast episodes that will hone in on a single problem. This time, it’s cannabis hyperemesis syndrome (aka Cannabinoid Hyperemesis Syndrome). Learn about the presentation, diagnosis, and treatment of this surprisingly common malady. PEMBlog.com Follow @PEMTweets on Twitter Check out the Facebook […]

Firearm Safety Oct 27, 2021

This episode was produced with Libby Ireson (@LibbyIreson on Twitter), Pediatric Resident at Cincinnati Children’s and is being released in conjunction with the 2021 Day of Action promoting firearm safety and speaking out against gun violence. The goals of this episode are to: Report statistics of pediatric firearm-related injuries/deaths in the United States Review the American Academy of Pediatrics’ recommendations on firearm safety […]

Concussions Sep 01, 2021

Concussions and closed head injuries are incredibly common in the Pediatric Emergency Department and in general Emergency Department, especially as we head into fall contact sports season. In this episode, featuring Brielle Stanton, MD, a Pediatric Emergency Medicine fellow from The UPMC Children’s Hospital of Pittsburgh, you will earn how to differentiate clinically important traumatic brain […]

Shoulder Dislocations Jul 22, 2021

What’s the best maneuver for reducing a dislocated shoulder? My guess is as good as yours. There are multiple maneuvers that work – and work well for anterior (AKA anterior-inferior) dislocations. This episode reviews how to manage shoulder dislocations in the Pediatric population. PEMBlog.com Follow me on Twitter @PEMTweets Check out the Facebook page References […]

Finger Dislocations Jul 15, 2021

It is much more common for children to break a finger than dislocate one. Why? Those darn growth plates. Nevertheless reducing a dislocated digit is one of the most common emergency procedures around and can generally be performed without much difficulty. However there are some situations where you shouldn’t just yank in the digit. Learn […]

Patella Dislocations Jul 07, 2021

Reducing a dislocated patella is super satisfying – both for the clinician and the patient. This episode reviews management of this common orthopedic concern so that you can perform a reduction maneuver without needing to call Orthopedics. PEMBlog.com Follow me on Twitter @PEMTweets Check out the Facebook page References Fithian DC,Paxton EW,Stone ML,Silva P,Davis DK,Elias […]

Nursemaid’s Elbow Jun 30, 2021

Never has there been a more anachronistic name for such a common malady. Hailing from the time when the wealthy had female domestic workers who cared for children within their large household, this outmoded eponym describes a common orthopedic condition that impacts young children. I’ll cast my vote for calling it “pulled elbow” like they […]

Adolescent sexual and reproductive health in the ED Jun 02, 2021

This episode features three members of the Pediatric Emergency Care Applied Research Network (PECARN) Adolescent Sexual Health Working Group. PECARN is a network that performs multicenter research related to the emergency care of children. The Adolescent Sexual Health Working Group is focused on researching topics of interest around sexual and reproductive health in the ED. […]

Magnet Ingestions May 19, 2021

This episode focuses on high-powered magnet ingestions in children and was a collaboration with Elizabeth Curtis – @egcurtismd and Libby Ireson – @LibbyIreson, two Categorical Pediatrics Residents at Cincinnati Children’s who served as producers and guest hosts. These rare earth magnets were briefly removed from the market because children swallowed them and, when two magnets attracted […]

Drowning May 12, 2021

With the warm weather upon us here in the Northern Hemisphere it will soon be time for the pools to open. This episode is therefore incredibly timely, and focuses on the spectrum of submersion injuries and their management. Learn about drowning physiology, when to admit to the hospital, and how to assess the child who […]

Toxicology Season 2 Episode 3: Nicotine Mar 16, 2021

This is Season 2 of the Toxicology podcast series that Seattle Childrens’ Toxicologist Suzan Mazor, MD and I put together. This three episode season turns its focus to drugs of abuse – continuing with this episode on nicotine toxicity – the final episode of this #ToxTuesdays season. I am now proud to offer CME through […]

Toxicology Season 2 Episode 2: Marijuana Mar 09, 2021

This is Season 2 of the Toxicology podcast series that Seattle Childrens’ Toxicologist Suzan Mazor, MD and I put together. It is a joint effort so to speak. This three episode season turns its focus to drugs of abuse – continuing with this episode on marijuana toxicity. So, let’s weed out the bad information, hash […]

Toxicology Season 2 Episode 1: Opioids Mar 02, 2021

This is Season 2 of the Toxicology podcast series that Seattle Childrens’ Toxicologist Suzan Mazor, MD and I put together. This three episode season turns its focus to drugs of abuse – beginning with this episode on opioid toxicity. So, slow your breathing, constrict your pupils, and focus in for the return of #ToxTuesdays. I […]

Return to sports following COVID-19 Feb 04, 2021

Even though we won’t be “clearing” patients in the ED we still need to be familiar with return to sports recommendations for children and adolescents who have had COVID-19. Remember, these are just recommendations and are based off of practice patterns at many centers and on the AAP guideline. Consult with your local hospital and […]

Hypertrophic pyloric stenosis Nov 12, 2020

Hypertrophic pyloric stenosis results from progressive thickening of the pyloric muscle, which leads to gastric outlet obstruction and vomiting in newborns. It is a can’t miss diagnosis and one of the most common surgical problems in newborns. Learn more about the diagnosis and management in this episode of PEM Currents: The Pediatric Emergency Medicine Podcast. […]

Toxicology Season 1 Episode 4: Salicylates Oct 13, 2020

This is episode four of season one of the Toxicology series that Suzan Mazor, the Medical Director for Toxicology at Seattle Children’s, and I are putting together. This episode focuses on a worrisome intentional and accidental ingestion – salicylates. Learn about diagnosis, management, and more! PEMBlog.com Follow me on Twitter @PEMTweets Check out the Facebook […]

Toxicology Season 1 Episode 3: Acetaminophen Oct 06, 2020

This is episode three of season one of the Toxicology series that Suzan Mazor, the Medical Director for Toxicology at Seattle Children’s, and I are putting together. This episode focuses on one of the most common intentional ingestions – Acetaminophen. For those of you from across the ocean – this episode tackles paracetamol, and for […]

Toxicology Season 1 Episode 2: Decontamination and Elimination Sep 29, 2020

This is episode 2 of season one of the Toxicology series that Suzan Mazor, the Medical Director for Toxicology at Seattle Children’s, and I are putting together. This follow up episode focuses on a decontamination and elimination in the poisoned pediatric patient and offers many pearls that will serve as a foundation for upcoming episodes […]

Toxicology Season 1 Episode 1: General approach to the poisoned patient Sep 22, 2020

This is episode 1 of season one of the Toxicology series that Suzan Mazor, the Medical Director for Toxicology at Seattle Children’s, and I are putting together. This premiere episode focuses on a solid general approach to the poisoned pediatric patient and offers many pearls that will serve as a foundation for upcoming episodes. Follow […]

Mastoiditis Jul 14, 2020

Does mastoiditis always present with the classic triad of swelling behind the ear, otalgia, and protrusion of the auricle? Do you need to get a CT to make the diagnosis? What is the exact relationship with acute otitis media? Can swimmer’s ear turn into mastoiditis? These questions and more are why I recorded this episode […]

Delirium Jun 09, 2020

Yes, PEM Currents is a Pediatric Emergency Medicine podcast, but during the COVID-19 pandemic we may be tasked with seeing patients outside of our area of expertise. Plus, there’s a lot we can learn from big people that we can extrapolate to children. I have partnered with POPCoRN, the Pediatric Overflow Planning Contingency Response Network to deliver […]

Multisystem Inflammatory Syndrome in Children May 21, 2020

Multisystem Inflammatory Syndrome in Children (MIS-C) is an evolving clinical entity that is occurring, possibly in association with or following a COVID-19 infection. This episode of PEM Currents expands upon a recent PEMBlog post, as well as includes information from two studies published in The Lancet as well as included in a recent CDC webinar. […]

Pulmonary Embolism May 14, 2020

Yes, PEM Currents is a Pediatric Emergency Medicine podcast, but during the COVID-19 pandemic we may be tasked with seeing patients outside of our area of expertise. Plus, there’s a lot we can learn from big people that we can extrapolate to children. I have partnered with POPCoRN, the Pediatric Overflow Planning Contingency Response Network to deliver […]

Vasopressors May 05, 2020

Vasopressor use in the Pediatric Emergency Department has been a moving target for my entire career. Back when I was a resident and fellow we used Dopamine. Then we went to epinephrine because it can be given through a peripheral IV because norepinephrine was too dangerous to run peripherally. But maybe that’s not entirely true. […]

Stroke in Adults Apr 22, 2020

Yes, PEM Currents is a Pediatric Emergency Medicine podcast, but during the COVID-19 pandemic we may be tasked with seeing patients outside of our area of expertise. Plus, there’s a lot we can learn from big people that we can extrapolate to children. I have partnered with POPCoRN, the Pediatric Overflow Planning Contingency Response Network to deliver […]

Status Epilepticus Mar 25, 2020

Status epilepticus can be very stressful in the Pediatric Emergency Department. This episode of PEM Currents: The Pediatric Emergency Medicine Podcast focuses on management, and will guide you through the treatment process, starting with benzodiazepines, followed by a discussion of the recent evidence for second line therapy between fosphenytoin, levetiracetam, and valproate. Follow me on […]

Hemophilia Feb 18, 2020

Factor First! OK, did I get your attention? Hopefully I did, because giving replacement factor to children with hemophilia presenting to the Emergency Department as soon as possible is the most important thing that you can do to positively impact outcomes. This episode of PEM Currents focuses on the different bleeding complications seen in Hemophilia […]

Talking with patients and families about the flu Dec 20, 2019

I recently had the pleasure of sitting down with the always delightful Dr. Patricia Chambers to talk about influenza. In our conversation we reviewed how to discuss testing or not for the flu, as well as why antivirals are not always indicated. I firmly believe that perhaps the most important thing that we do in […]

Disaster Preparedness Oct 25, 2019

This episode of PEM Currents: The Pediatric Emergency Medicine Podcast is all about disaster medicine. I interviewed Brent Kaziny, Disaster Medicine and Preparedness expert who was in training during Hurricane Katrina and lead efforts in Houston during Hurricane Harvey. Brent shares practical tips on how you can get involved and how you can learn what […]

Foot Fractures Sep 27, 2019

Don’t toe the line when it comes to your education. Step up, don’t be a heel, and listen to this episode of PEM Currents: The Pediatric Emergency Medicine Podcast focusing on fractures of the feet and toes. Learn all about metatarsal fractures, including the Jones fracture, Lisfranc injuries, why you should worry about a fracture […]

Femur Fractures Sep 20, 2019

The fifth episode of the Fracture Season of PEM Currents, the Pediatric Emergency Medicine podcast focuses on fractures of the tibia and fibula, including the ankle. This episode also features a review of the neurovascular assessment of the lower extremity. I am now proud to offer CME through Cincinnati Children’s. To claim CME & ABP […]

Tibia and Fibula Fractures Sep 13, 2019

The fifth episode of the Fracture Season of PEM Currents, the Pediatric Emergency Medicine podcast focuses on fractures of the tibia and fibula, including the ankle. This episode also features a review of the neurovascular assessment of the lower extremity. I am now proud to offer CME through Cincinnati Children’s. To claim CME & ABP […]

Hand Fractures Sep 06, 2019

This is the 4th episode in the Fracture Season of PEM Currents. You will learn about carpal fractures – especially the dreaded scaphoid fracture, metacarpal fractures, and fractures of the phalanges. I am now proud to offer CME through Cincinnati Children’s. To claim CME & ABP MOC Part 2, visit Cincinnati Children’s Online Courses and search ‘PEM […]

Humerus Fractures Aug 30, 2019

This episode in the Fracture Season of PEM Currents, the Pediatric Emergency Medicine podcast focuses on humerus fractures. The humerus is a super duper forgiving bone in pediatrics that almost never requires reduction or surgeries if there is a mid shaft or proximal shaft fracture. Don’t forget to listen to the Forearm and Wrist Episode […]

Elbow Fractures Aug 23, 2019

This episode in the Fracture Season of PEM Currents, the Pediatric Emergency Medicine podcast focuses on elbow fractures. Did you know that the elbow has there joints? Did you know that supracondylar fractures can happen after a fall from something other than monkey bars? Don’t forget to listen to the Forearm and Wrist Episode if […]

Forearm and Wrist Fractures Aug 16, 2019

This summer, in honor of the 7th anniversary of PEMBlog and PEM Currents I will be releasing a mini-season of fracture focused podcasts. This episode focuses on radius and ulna fractures, including buckle, greenstick, physis and more! learn about the neurovascular assessment of the upper extremity and general management pearls for some of the most […]

SVT Jun 04, 2019

Three of my favorite letters in the Pediatric Emergency Department are S, V and T. This episode of PEM Currents, the Pediatric Emergency Medicine Podcast focus on the diagnosis and management of paroxysmal supraventricular tachycardia in the ED. I discuss preparation, vagal maneuvers, cardioversion, disposition and more! PEMBlog.com @PEMTweets on Twitter Facebook References Appelboam, et […]

Measles May 14, 2019

I never thought that this particular disease would make a comeback in the United States. But here we are. Measles. As of May 2019 there have been cases reported in over 20 states. Declining vaccine rates and international travel to areas with local measles epidemics have led to a sharp rise in the number of […]

Constipation Mar 13, 2019

Constipation is an incredibly common problem in the Pediatric Emergency Department and amongst children who visit the Emergency Department with complaints of abdominal pain. This episode of PEM Currents, the Pediatric Emergency Medicine podcast features an interview with Danny Mallon, a Gastroenterologist from Cincinnati Children’s @dannymallon24 who is an expert in managing pediatric constipation. Our discussion […]

Anaphylaxis: Admit or Discharge? Feb 20, 2019

You will no doubt see a child with anaphylaxis in the Emergency Department. Recognition, management and disposition are all key questions that feel incredibly fluid at this juncture. I had the pleasure of interviewing Tim Dribin, an Emergency Medicine Attending from Cincinnati Children’s who recently published a paper in PLUS ONE focusing on admissions for […]

Sinusitis Jan 30, 2019

Did you know that up to 9% of URIs are eventually complicated by acute sinusitis in children? This episode of PEM Currents, the Pediatric Emergency Medicine podcast focuses on making the diagnosis of acute bacterial rhinosinusitis clinically and when to pull the antibiotic prescription trigger. PEMBlog.com @PEMTweets References Chow AW, Benninger MS, Brook I, Brozek […]

Testicular Pain Jan 22, 2019

Acute testicular pain is a common presenting complaint in the Pediatric Emergency Department. In this episode of PEM Currents you will learn about testicular torsion, epididymitis, torsion of the appendix testis and appendix epididymis, inguinal hernias and more. And remember, first and foremost, time is testicle! PEMBlog.com @PEMTweets References Jefferies MT, Cox AC, Gupta A, […]

Probiotics for Gastroenteritis Dec 12, 2018

This episode of PEM Currents features an in-depth interview with the lead author on the recent New England Journal paper on the use of probiotics in gastroenteritis. David Schnadower was kind enough to sit down with me and James Gray, a Pediatric Emergency Medicine Fellow from Cincinnati Children’s to talk about the study and its […]

Intranasal Ketamine Nov 02, 2018

I am delighted to bring you this special episode of PEM Currents, the Pediatric Emergency Medicine podcast. It’s all about intranasal ketamine and its use for acute pain management in the Pediatric Emergency Department. I had the pleasure of interviewing Theresa Frey, Assistant Professor from the Division of Emergency Medicine at Cincinnati Children’s. Theresa is […]

Pelvic Avulsion Fractures Oct 19, 2018

Pop goes the apophysis! In teenage athletes the apophyseal cartilage is the weak point along the pelvic rim. Learn about these common injuries in this edition of PEM Currents, the Pediatric Emergency Medicine podcast. Find more great educational content at PEMBlog Follow me on Twitter @PEMTweets References Kocher MS, Tucker R. Pediatric athlete hip disorders. R.Clin Sports […]

Acute Flaccid Myelitis Oct 18, 2018

Acute Flaccid Myelitis is a rare but serious disease characterized by rapid onset of muscle weakness. Diagnosis also requires an MRI with lesions in multiple spinal levels or CSF pleocytosis. cases have been reported over the past several years and though a specific cause is unknown strains of enterovirus are suspected culprits. Check out more […]

Otitis Externa Jul 25, 2018

With summer pool season in full swing allow me to freestyle a little on a common topic that many Emergency Departments and Urgent Cares seem to be swimming in every summer. This episode of PEM Currents dives right into Otitis Externa – AKA Swimmer’s Ear and reviews diagnosis and treatment. If you were treading water […]

Kawasaki Disease May 15, 2018

Kawasaki Disease, AKA Mucocutaneous Lymph Node Syndrome, is one of the most common vasculitides of childhood. The hallmark is fever ≥5 days plus 4/5 of the following; mucous membrane changes, conjunctivitis, polymorphous rash, extremity changes and lymph node enlargement. It can also lead to coronary artery aneurysms, which is why its so important to make […]

Acute Otitis Media Apr 13, 2018

OK, so this is the least exciting topic in Pediatric Emergency Medicine… With that being said, you will all see it. And we need to be good at looking at ears, diagnosing acute otitis media, and appropriately choosing when and which antibiotic to prescribe. Follow @PEMTweets on Twitter References Karma PH, et al., Pneumatic otoscopy […]

Dental Infections Feb 20, 2018

To tell you the tooth you’ll probably see quite a few kids with dental related complaints in the Pediatric Emergency Department. This can range from cavities to invasive infections. Brush up on all things dental infections in this episode of PEM Currents. And yes, those puns were intentional. I must’ve flossed my mind! PEMBlog Briefs: […]

Testing for Influenza Jan 29, 2018

You don’t need a flu test to diagnose the flu! But there are situations where rapid antigen testing or PCR is valuable. Listen to this episode of PEM Currents, the Pediatric Emergency Medicine podcast, to learn more about the test characteristics of common assays and when to obtain testing when prevalence rates for the flu […]

Hyperkalemia Dec 27, 2017

Hyperkalemia is more than just peaked T-waves on an EKG. Learn why an elevated serum potassium level can put patients in the danger zone and how to acutely manage patients in a goal directed manner. Check out more great educational content on PEMBlog.com Follow me on Twitter @PEMTweets

Bronchiolitis Nov 01, 2017

I’m sure that you’ll probably see a case of bronchiolitis this winter. Call it a hunch. In this episode of PEM Currents you’ll learn why suctioning and ensuring hydration are still the mainstays of therapy, and why albuterol, racemic epinephrine, steroids and more don’t have a place in routine cases. And if you read any […]

Rapid Sequence Intubation Sep 29, 2017

This episode of PEM Currents, featuring Preston Dean – @prestonndean on Twitter, a senior Pediatric Resident at Cincinnati Children’s, is about all things Rapid Sequence Intubation. You’ll learn about equipment, techniques, drugs and more! PEMBlog.com

Community Acquired Pneumonia Sep 20, 2017

Fever, tachypnea and rales – it must be a community acquired pneumonia… right? Learn more about the diagnosis and management of this common problem in the Pediatric Emergency Department. Essential Reading Bradley JS, Byington CL, Shah SS, Alverson B, Carter ER, Harrison C, Kaplan SL, Mace SE, McCracken GH Jr, Moore MR, St Peter SD, […]

CSF Shunt Complications Aug 18, 2017

Ventricular CSF shunts are very common – many kids have them. The most common complications are malfunction and infection. This episode of PEM Currents reviews the basics and how you can assess for complications in CSF shunts in kids. PEMBlog.com Boyle, Kimia, Nigrovic. Validating a Clinical Prediction Rule for Ventricular Shunt Malfunction. Pediatric Emergency Care, 2017. […]

Vocal Cord Dysfunction May 25, 2017

Vocal cord dysfunction, AKA paradoxical vocal fold motion is more common than you might think. Patients often present to the Emergency Department in respiratory distress and “wheezing.” Learn about the diagnosis itself, different phenotypes and what treatment options are out there. References Christopher KL, Wood RP 2nd, Eckert RC, Blager FB, Raney RA, Souhrada JF. Vocal-cord dysfunction […]

Management of Elevated ICP May 05, 2017

Get ahead of your peers and listen to this episode of PEM Currents, the Pediatric Emergency Medicine podcast where you’ll learn all about the management of acutely elevated intracranial pressure. You’ll learn about common maneuvers such as optimizing the ABCs, Keeping the head elevated and midline as well as thermoregulation. I also discuss osmotic therapies […]

Breath Holding Spells Mar 22, 2017

Don’t hold you breath while listening to this podcast – because you’d be doing so for longer than 20 seconds – and you will have apnea. Do however, listen to learn more about cyanotic and pallid breath holding spells so that you can be prepared to diagnose and manage them in the Emergency Department. Check […]

Serum sickness Jan 31, 2017

What does the combination of erythema multiforme, fever and swollen joints equal? If you answered a visit to the Emergency Department you’re only partially correct. Serum sickness like reaction is a delayed type hypersensitivity reaction that often occurs 7-10 days after starting a course of antibiotics. Learn how you can recognize it and differentiate it […]

Kidney Stones Jan 03, 2017

It’s an epidemic! OK, so not quite, but we are seeing a rise in the number of kidney stones recently and we’re not quite sure why. This episode of PEMCurrents will focus on diagnosis and treatment of stones and answer such questions as; Which pain medicine should I order first? and which is the better imaging […]

Hemorrhagic Ovarian Cysts Dec 13, 2016

Check out the latest episode of PEM Currents the Pediatric Emergency Medicine podcast where I talk about hemorrhagic (AKA ruptured) ovarian cysts. I delve into diagnosis and management and suggest strategies for obtaining a diagnostic ultrasound. Check out more great educational content on PEMBlog.com

Interview with Ben Kerrey about Pediatric Rapid Sequence Intubation Oct 21, 2016

Ben Kerrey is a rising star in Pediatric Emergency Medicine and is the point man for an ongoing initiative at Cincinnati Children’s centered around improving safety and limiting complications during rapid sequence intubation. I recently sat down with Ben to talk about the state of RSI in pediatric patients, the difference between a checklist and a […]

Rabies Sep 23, 2016

This edition of PEM Currents is a bite-sized rundown on rabies, or more accurately rabies post-exposure prophylaxis since most of you will never see it clinically, but will encounter a kid who meets an unscrupulous animal.

Hematemesis in the Newborn Sep 06, 2016

Hematemesis in the newborn period is scary for parents but fortunately it is most often due to benign causes such as swallowed maternal blood or GERD. learn more about this surprisingly common problem on this edition of PEMCurrents, the Pediatric Emergency Medicine Podcast.

Heat Illness Jun 21, 2016

The heat is on! With warm weather comes a plethora of heat-related problems in the ED. That’s why I’m sharing this edition of PEM Currents, the Pediatric Emergency Medicine Podcast. The focus is on heat illness in its many forms. Learn about everything from the benign prickly heat, to life threatening heat stroke. Stay cool and learn […]

Swallowed Foreign Bodies Jun 10, 2016

Kids eat stuff they’re not supposed to. Most of the time foreign bodies pass harmlessly through the GI tract. Occasionally they will get stuck. It is your job to figure out who has an impacted foreign body, and how to diagnose and manage it. Check out more Pediatric Emergency Medicine content at PEMBlog.com Follow me […]

Torticollis May 03, 2016

Acquired torticollis must be differentiated from more serious symptoms and remains a common presenting complaint in the Pediatric Emergency Department. Learn more about it in this episode of PEMCurrents the Pediatric Emergency Medicine podcast.

Strep Pharyngitis Feb 24, 2016

This may be a bit hard to swallow, but not every disease process in the Emergency Department is exciting. Streptococcal pharyngitis is an incredibly common condition, especially in the Pediatric Emergency Department and I wanted to take this opportunity to answer some common questions. Who knows, perhaps after listening to this edition of PEM Currents you […]

Respiratory Distress Nov 17, 2015

Take a deep breath and PEEP this – PEM Currents, the Pediatric Emergency Medicine podcast proudly brings you an episode dedicated to the initial assessment and management of respiratory distress. Whether you’ve been practicing in the field for 20 years or are fresh out of medical school it is important to recognize key symptoms in […]

ITP Oct 06, 2015

This edition of PEM Currents, the Pediatric Emergency Medicine Podcast™ reviews the diagnosis and management of Immune Thrombocytopenia, formerly known as Idiopathic Thrombocytopenia Purpura. You will definitely see this common acute hematologic conditions in the ED, and should be able to differentiate it from acute leukemia, meningococcemia and other concerning conditions.

Unexplained Bruising in the Young Child Sep 08, 2015

This edition of PEM Currents, the Pediatric Emergency Medicine podcast briefly addresses which bruises are concerning in children under the age of 4, and what the ensuing workup should entail. You can also read more on a companion PEMBlog post.

The Febrile Newborn Jul 06, 2015

This episode of PEM Currents tackles a bread and butter issue in Pediatric Emergency Medicine, the newborn with fever. I discuss management, specifically how it differs for babies under 28 days of age as well as when to get labs and how to interpret them. I also reference procalcitonin, and touch on its emerging role. […]

Upper Gastrointestinal Tract Bleeds Jun 02, 2015

This episode focuses on upper GI bleeds. Serious UGI bleeds – you know, the ones with shock, massive transfusions and more – are fortunately rare in the Pediatric Emergency Department. However, there is a growing population of patients with chronic diseases that can lead to portal hypertension, varies and other causes of bleeding from the […]

An interview with Todd Florin on bronchiolitis, hypertonic saline and more Mar 09, 2015

I’m delighted to share the latest PEM Currents podcast! I recently sat down with Todd Florin, one of the faculty physicians at Cincinnati Children’s Hospital Medical Center and talked about bronchiolitis, delving into the controversies around the use of hypertonic saline, albuterol and more. Todd also recommended that all of my listeners check out the […]

Parotitis Jan 14, 2015

With the recent influenza epidemic you may have also seen a rise in the number of cases of parotitis. This should not be a surprise, as acute parotitis is usually viral, self-limited and treated with supportive measures – just like the flu! Learn more by listening to this edition of PEM Currents, which is all […]

Topical Anesthetics Oct 12, 2014

PEM Currents returns with a look at topical anesthetics used in the Emergency Department. Specifically this edition of the podcast will focus on LET, EMLA and LMX and discuss typical use.

Convulsive syncope Aug 11, 2014

Don’t swoon with excitement because the latest episode of PEM Currents, the Pediatric Emergency Medicine podcast is here! The focus is on convulsive syncope – essentially patients who faint and have movements that could be construed as seizures. You’ll learn how common convulsions with syncope are and what to do if you encounter them in […]

Acetaminophen versus Ibuprofen May 29, 2014

This edition of PEM Currents, the Pediatric Emergency Medicine podcast, reviews the safety and comparative efficacy of acetaminophen and ibuprofen. If you work in a Pediatric Emergency Department you’ll certainly have broken a sweat over this hot debate time and time again.

Ondansetron for vomiting in acute gastroenteritis May 03, 2014

This edition of PEMCurrents echoes a recent post on the PEMBlog and reviews the use of ondansetron in acute gastroenteritis. Specifically highlighting the reduction in risk of further episodes of emesis, need for intravenous fluids and immediate admission to the hospital.

Clavicle Fractures Apr 28, 2014

This edition of PEMCurrents takes a crack at clavicle fractures. The old dictum about broken collarbones states that if both ends of the bone are in the same room it’ll heal fine. For the most part this is true – at least in prepubescent patients. New literature in adults has suggested that outcomes are better […]

Antibiotic Therapy for Osteomyelitis Mar 13, 2014

Recognizing osteomyelitis can be challenging. Treating it doesn’t have to be – especially in the Pediatric ED. This edition of PEM Currents reviews the current evidence surrounding the initial choice of antibiotic, monitoring treatment response and overall therapeutic duration.

Antiemetics for Migraines Mar 02, 2014

This edition of PEM Currents focuses on the use of antiemetics to treat status migrainosus in the Pediatric ED. Prochlorperazine and Metoclopramide are safe and effective agents with a low incidence of self limited side effects that when given in combination with ketorolac result in over 90% of patient being headache free at 3 hours. […]

Retropharyngeal Abscesses Dec 12, 2013

Ted Brenkert sticks his neck out to educate you on retropharyngeal abscesses. RPAs can be an especially worrisome diagnosis in young children who will present with fever, sore throat and limitation of neck movement. Check out pemblog.com for more educational content

High Flow Dec 05, 2013

This episode of PEMCurrents is narrated by Brad Sobolewski and focuses on the use of high flow in bronchiolitis. Learn about the application of high flow nasal cannulas, the mechanism behind their generation of positive airway pressure, as well as some of the literature behind its beneficial effects. Check out pemblog.com for more educational content

Dental Trauma Sep 27, 2013

PEM Currents cuts to the tooth of the matter in an effort to help you brush up on dental trauma. Ted Brenkert has been chomping at the bit to fill the cavities in your brain with useful knowledge.

Forearm fractures Aug 09, 2013

Grab your BBFF (or BFF) and FOOSH your way on over to PEM Currents for a discussion surrounding forearm fractures, one of the most common Orthopedic injuries seen in the Pediatric ED.

Ketamine Jul 25, 2013

Summertime is in full swing – so you know what that means. Lacerations, broken bones, other stuff – and a lot of sedations to do. This edition of PEM Currents focuses on Ketamine and its use as the primary agent for procedural sedation in the Pediatric ED.

Summer Penile Syndrome Jul 10, 2013

PEM Currents returns with a second episode focusing on a rather “private” matter. Summer penile syndrome is a hypersensitivity reaction to an insect bite (usually a chigger) that causes pruritis and edema to the skin of the penile shaft. This episode reviews the diagnosis and management of this surprisingly common clinical entity.

Grudge match! Dexamethasone versus prednisone in acute asthma Jan 08, 2013

Welcome to the first podcast in the PEMCurrents series. Ted Brenkert discusses the use of dexamethasone versus prednisone in acute asthma exacerbations in the ED. You can access the podcast on iTunes, or if you’d like download the file directly. We welcome any and all feedback in the comments section. Here are links to pdf […]

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PEM Currents: The Pediatric Emergency Medicine Podcast

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Emily Groopman, MD, PhD

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